pituitrin and Hypoglycemia

Osmotic demyelination of the brain (ODS) is a dreaded complication that typically occurs several days after aggressive therapy for chronic hyponatraemia, but is eminently avoidable. In this teaching exercise, Professor McCance, an imaginary consultant, is asked to explain how he would have treated a 28-year-old female who had hyperkalaemia, hypoglycaemia, hypotension and hyponatraemia (118 mM) to prevent the development of ODS. He begins with a review of the physiology, including his own landmark work on chronic hyponatraemia associated with a contracted extracellular fluid volume. Adding quantitative analysis, the cause of the excessive rise in plasma sodium concentration is revealed, and a better plan for therapy is proposed.

Topics: Addison Disease; Adult; Brain Diseases; Demyelinating Diseases; Female; Humans; Hyperkalemia; Hypoglycemia; Hyponatremia; Hypotension; Renal Agents; Syndrome; Vasopressins; Water-Electrolyte Imbalance

A survey is given on the regulation of the formation of corticoliberin and of pro-opiomelanocortin and of ACTH, respectively, and on the significance of these compounds. The formation of pro-opiomelanocortin is furthered by corticoliberin, vasopressin, oxytocin and angiotensin II. Receptors for the binding of corticoliberin appear in numerous parts of the central nervous system. In various diseases the content of corticoliberin in the plasma and in certain tissues is changed. The inhibition of the ACTH secretion by glucocorticosteroids takes place via a decrease of the formation of corticoliberin and by a reduction of the equipment of the corticotrophic cells with receptors for its binding. The secretion of corticoliberin and of ACTH, respectively, is increased by loads, by hypoglycaemia, by blood losses, by hypoxia and by infections. In the glucocorticosteroid receptors there are 2 types with different affinity to cortisol and corticosterone.

Topics: Adrenocorticotropic Hormone; Angiotensin II; Corticotropin-Releasing Hormone; Hemorrhage; Humans; Hypoglycemia; Hypoxia; Infections; Oxytocin; Pro-Opiomelanocortin; Receptors, Cell Surface; Vasopressins

The functional characteristics of osmoregulated vasopressin secretion can be defined in terms of an osmotic threshold for its release and a sensitivity of the osmoreceptor and vasopressin-secreting unit. Osmotically stimulated thirst has features similar to osmoregulated vasopressin. There are wide individual variations in the functional characteristics of both thirst and vasopressin release in healthy humans, probably genetic in origin. The influence of aging appears to enhance the sensitivity of vasopressin secretion but blunt thirst appreciation. Yet in many physiological situations changes in osmoregulated vasopressin release and thirst occur in parallel. The fall in plasma osmolality associated with human pregnancy is accounted for entirely by a lowering of the osmotic thresholds for thirst and vasopressin release. Similar but less marked alterations accompany the ovulatory luteal phase of the menstrual cycle. A major nonosmotic stimulus to vasopressin secretion is hypotension and/or hypovolemia, mediated by high- (carotid sinus) and low- (left atrial) pressure receptors. Circulating catecholamines influence the release of vasopressin by alpha- and beta-adrenergic pathways. Drinking by hypertonic humans provides immediate reduction in thirst and vasopressin secretion probably mediated by pathways from the oropharynx. The modest but variable rise in plasma vasopressin in response to hypoglycemia appears to be due to cellular neuroglycopenia and is independent of parasympathetic pathways. Although osmotic and hemodynamic stimuli to vasopressin release do not act independently of each other, the precise subtle interactions between them and other nonosmotic stimuli remain to be clarified.

Topics: Drinking; Humans; Hypoglycemia; Nausea; Pressoreceptors; Thirst; Vasopressins; Vomiting; Water-Electrolyte Balance

Topics: Adrenocorticotropic Hormone; Calcitonin; Erythropoietin; Gonadotropins; Growth Hormone; Hormones, Ectopic; Humans; Hypercalcemia; Hypoglycemia; Neoplasms; Neurophysins; Oxytocin; Paraneoplastic Endocrine Syndromes; Parathyroid Hormone; Peptides; Placental Lactogen; Prolactin; Radioimmunoassay; Receptors, Cell Surface; Thyrotropin; Vasopressins

Topics: Adrenocorticotropic Hormone; Chorionic Gonadotropin; Cushing Syndrome; Erythropoietin; Gastrointestinal Hormones; Hormones, Ectopic; Hypercalcemia; Hypoglycemia; Hyponatremia; Melanocyte-Stimulating Hormones; Neurologic Manifestations; Paraneoplastic Endocrine Syndromes; Parathyroid Hormone; Polycythemia; Prostaglandins E; Somatomedins; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adrenal Cortex; Adrenal Glands; Adrenocorticotropic Hormone; Anorexia Nervosa; Blood Glucose; Brain Diseases; Catecholamines; Child; Circadian Rhythm; Cyproterone; Dexamethasone; Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Hypothalamus; Infant; Insulin; Metyrapone; Nephrotic Syndrome; Obesity; Pituitary Gland; Prednisone; Vasopressins

Topics: 5-Hydroxytryptophan; Acanthosis Nigricans; Carcinoid Tumor; Carotid Body Tumor; Catecholamines; Cushing Syndrome; Dermatomyositis; Endocrine System Diseases; Gynecomastia; Hormones, Ectopic; Humans; Hypercalcemia; Hyperthyroidism; Hypoglycemia; Hyponatremia; Neoplasms; Neuromuscular Diseases; Osteoarthropathy, Secondary Hypertrophic; Peripheral Nervous System Diseases; Polycythemia; Puberty, Precocious; Syndrome; Toxins, Biological; Vascular Diseases; Vasopressins; Zollinger-Ellison Syndrome

Topics: 5-Hydroxytryptophan; Adrenocorticotropic Hormone; Chorionic Gonadotropin; Gastrins; Hormones, Ectopic; Humans; Hypercalcemia; Hypoglycemia; Neoplasms; Parathyroid Hormone; Precancerous Conditions; Thyrotropin; Vasopressins

Topics: Adrenocorticotropic Hormone; Endocrine System Diseases; Erythropoietin; Gynecomastia; Hormones, Ectopic; Humans; Hypercalcemia; Hyperthyroidism; Hypoglycemia; Hyponatremia; Insulin; Luteinizing Hormone; Melanocyte-Stimulating Hormones; Neoplasms; Parathyroid Hormone; Polycythemia; Puberty, Precocious; Thyrotropin; Vasopressins

Early sleep in humans is characterized by a distinct suppression of pituitary-adrenal activity coinciding with enhanced activity of the somatotropic axis. Here, we tested in awake humans the hypothesis of an inhibiting influence of hypothalamic growth hormone-releasing hormone (GHRH) on pituitary-adrenal activity. For this purpose, pituitary-adrenal activity was stimulated in 10 men through a standard insulin-hypoglycemia-test (IHT) and in another 10 men through combined administration of CRH/vasopressin. Stimulation was performed in each man on three conditions following pretreatment with Placebo and GHRH administered intravenously (50 microg) or intranasally (300 microg) 1 h before. GH, ACTH and cortisol as well as blood pressure and heart rate were measured repeatedly. Contrary to expectations, pretreatment with GHRH did not suppress but enhanced secretion of cortisol upon insulin-induced hypoglycemia regardless of the route of GHRH pretreatment (p<0.05). In contrast, GHRH did not facilitate cortisol release after stimulation with CRH/vasopressin. Changes in ACTH remained inconsistent. Plasma levels of GH increased significantly after i.v. GHRH application, but remained unchanged after the intranasal administration. Blood pressure and heart rate were not influenced by the treatments. Results indicate facilitating effects of GHRH mediated at a suprapituitary (i.e. hypothalamic) level as suggested by restriction of the effect to the hypoglycemia-induced cortisol release with no effects after pituitary stimulation with CRH/vasopressin.

Topics: Administration, Intranasal; Adrenal Glands; Adrenocorticotropic Hormone; Adult; Affect; Blood Glucose; Blood Pressure; Corticotropin-Releasing Hormone; Growth Hormone-Releasing Hormone; Heart Rate; Human Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Injections, Intravenous; Insulin; Male; Pituitary Gland; Vasopressins

Leptin, produced by adipocytes, has homeostatic effects on body fat mass through inhibition of appetite and stimulation of the sympathetic nervous system. Several studies have reported that high-dose exogenous glucocorticoids increase circulating leptin concentrations in humans. Conversely, leptin has inhibitory effects on the hypothalamic-pituitary-adrenal (HPA) axis, both at the hypothalamic and adrenal levels. We hypothesized that acute hypercortisolism, in the physiological range, may not alter leptin secretion. Four stimuli of the HPA axis were administered to eight healthy male volunteers in a placebo-controlled study. On separate afternoons, in a randomised order, fasting subjects received i.v. injections of saline, naloxone (125 microg/kg); vasopressin (0.0143 IU/kg); naloxone and vasopressin in combination; or insulin (0.15 U/kg; a dose sufficient to induce hypoglycaemia). Plasma concentrations of adrenocorticotrophic hormone (ACTH), cortisol and leptin were measured before and for 120 min after the injection. The cortisol secretory response was greatest after insulin-hypoglycaemia, this response was significantly greater than that following naloxone, naloxone/vasopressin, or vasopressin alone. Despite the cortisol release, leptin concentrations were not increased after any stimulus. Insulin-hypoglycaemia was associated with a decrease in leptin concentration at 60 and 90 min, while naloxone did not alter leptin concentrations. However, basal leptin concentrations were positively correlated with integrated ACTH and cortisol responses to naloxone, but did not correlate with ACTH or cortisol responses to the other stimuli. Thus acute elevations of plasma cortisol, in the physiological range, do not appear to influence plasma leptin concentrations. The fall in plasma leptin concentration after insulin-induced hypoglycaemia may reflect catecholamine secretion after this stimulus.

Topics: Adrenocorticotropic Hormone; Adult; Humans; Hydrocortisone; Hypoglycemia; Hypoglycemic Agents; Hypothalamo-Hypophyseal System; Insulin; Leptin; Male; Middle Aged; Naloxone; Narcotic Antagonists; Pituitary-Adrenal System; Vasoconstrictor Agents; Vasopressins

Topics: Adrenocorticotropic Hormone; Electric Stimulation Therapy; Humans; Hypoglycemia; Insulin; Pneumoencephalography; Vasopressins

The counterregulatory response to hypoglycemia (CRR), which ensures a sufficient glucose supply to the brain, is an essential survival function. It is orchestrated by incompletely characterized glucose-sensing neurons, which trigger a coordinated autonomous and hormonal response that restores normoglycemia. Here, we investigate the role of hypothalamic Tmem117, identified in a genetic screen as a regulator of CRR. We show that Tmem117 is expressed in vasopressin magnocellular neurons of the hypothalamus. Tmem117 inactivation in these neurons increases hypoglycemia-induced vasopressin secretion leading to higher glucagon secretion in male mice, and this effect is estrus cycle phase dependent in female mice. Ex vivo electrophysiological analysis, in situ hybridization, and in vivo calcium imaging reveal that Tmem117 inactivation does not affect the glucose-sensing properties of vasopressin neurons but increases ER stress, ROS production, and intracellular calcium levels accompanied by increased vasopressin production and secretion. Thus, Tmem117 in vasopressin neurons is a physiological regulator of glucagon secretion, which highlights the role of these neurons in the coordinated response to hypoglycemia.

Topics: Animals; Blood Glucose; Calcium; Female; Glucagon; Glucose; Hypoglycemia; Insulin; Male; Mice; Neurons; Vasopressins

In vasopressin-deficient rat pups stressor-induced adrenocorticotropin (ACTH) and corticosterone elevations markedly dissociate. We have shown recently that during the postnatal period mineralocorticoid secretion is more sensitive to stressor exposure than that of glucocorticoids. We have therefore hypothesized that in vasopressin-deficient pups during hypoglycemia, a stressor triggering aldosterone release mainly via ACTH, aldosterone release will change in parallel with ACTH. An additional aim was to reveal at which stage of the development occurs the shift from aldosterone to corticosterone as primarily stressor-induced adrenocortical hormone.. Vasopressin-deficient (di/di) and control Brattleboro rats were used both postnatally (10-day-old rats) and in adulthood.. Hypoglycemia induced similar ACTH elevations in pups and adults with significantly lower levels in di/di rats. In contrast, vasopressin-deficiency resulted in elevated resting aldosterone and stressor-induced corticosterone levels in pups without genotype differences in adults. Thus, aldosterone levels also dissociated from ACTH secretion. During stress, pups showed only minimal corticosterone increase, with relatively high aldosterone elevation. Resting levels of gluco- and mineralocorticoid receptor mRNA were smaller, while corticosterone-deactivating enzyme (11β-HSD2) mRNA level were higher in the hippocampus of 10-day-old rats compared to adults.. AVP does not seem to substantially regulate the stressor-induced aldosterone production, but both hormones contribute to salt-water regulation. Postnatally higher stressor-induced aldosterone than corticosterone production was still detectable in 40-day-old rats, although to a lesser extent, supporting a shift in the balance between stressor-induced glucocorticoid and mineralocorticoid hormone release throughout the development occurring in rats after postnatal day 40.

Topics: Adrenocorticotropic Hormone; Aldosterone; Animals; Corticosterone; Gene Deletion; Hypoglycemia; Male; Rats, Brattleboro; Stress, Psychological; Vasopressins

Activation of central type II glucocorticoid receptors (GR) during neutral protamine Hagedorn insulin (NPH) administration exacerbates recurring hypoglycemia. The hypothalamic paraventricular nucleus (PVN) integrates metabolic sensory input, controls autonomic and neuroendocrine motor outflow, and is characterized by abundant GR expression. The present studies investigated the hypothesis that PVN GR mediate intensification of hypoglycemia by serial NPH dosing, and that PVN glucokinase (GCK) and glucoregulatory neuropeptide genes acclimate to this treatment paradigm through GR-dependent mechanisms. Groups of adult male rats were injected subcutaneously with one or four doses of NPH, on as many days, while controls received vehicle. Bilateral administration of the selective GR antagonist, CP-472555, into the PVN prior to the first three NPH injections prevented amplification of hypoglycemia in response to the final insulin dose, while intra-PVN delivery of the GR agonist, dexamethasone, to euglycemic rats did not modify ensuing NPH-induced hypoglycemia. Quantitative real-time RT-PCR analysis of microdissected PVN tissue revealed that GCK, corticotropin-releasing hormone (CRH), oxytocin (OT), and vasopressin (VP) mRNA levels were unchanged in response to acute NPH, and baseline gene profiles measured 24 h after antecedent injections were similar to vehicle controls. In contrast, serial dosing with NPH elevated CRH and GCK, diminished OT, but did not alter VP gene transcripts. Intracerebroventricular CP-472555 delivery in conjunction with antecedent NPH dosing prevented transcriptional habituation of GCK and OT genes, but did not modify CRH or VP mRNA profiles. The present data show that activation of PVN GR during antecedent intermediate insulin-induced hypoglycemia is required for exacerbation of recurring hypoglycemia, and receptor stimulation in the absence of hypoglycemia and/or its sequelae does not intensify the effects of subsequent NPH administration. The results also provide evidence for acclimation of PVN CRH, GCK, and OT gene profiles to serial NPH dosing, and demonstrate that GR may be involved in GCK and OT transcriptional adaptation to ongoing intermediate insulin-induced hypoglycemia.

Topics: Animals; Corticotropin-Releasing Hormone; Dexamethasone; Gene Expression Profiling; Gene Expression Regulation; Glucokinase; Hypoglycemia; Injections, Intraventricular; Insulin, Isophane; Male; Neuropeptides; Oxytocin; Paraventricular Hypothalamic Nucleus; Phenanthrenes; Pyridines; Rats; Receptors, Glucocorticoid; RNA, Messenger; Transcriptional Activation; Vasopressins

A limiting factor to the clinical management of diabetes is iatrogenic hypoglycemia. With multiple hypoglycemic episodes, the collective neuroendocrine response that restores euglycemia is impaired. In our animal model of recurrent hypoglycemia (RH), neuroendocrine deficits are accompanied by a decrease in medial hypothalamic activation. Here we tested the hypothesis that the medial hypothalamus may exhibit unique changes in the expression of regulatory proteins in response to RH. We report that expression of the immediate early gene FosB is increased in medial hypothalamic nuclei, anterior hypothalamus, and posterior paraventricular nucleus of the thalamus (THPVN) of the thalamus following RH. We identified the hypothalamic PVN, a key autonomic output site, among the regions expressing FosB. To identify the subtype(s) of neuronal populations that express FosB, we screened candidate neuropeptides of the PVN for coexpression using dual fluorescence immunohistochemistry. Among the neuropeptides analyzed [including oxytocin, vasopressin, thyrotropin-releasing hormone, and corticotropin-releasing factor (CRF)], FosB was only identified in CRF-positive neurons. Inhibitory gamma-aminobutyric acid-positive processes appear to impinge on these FosB-expressing neurons. Finally, we observed a significant decrease in the presynaptic marker synaptophysin within the PVN of RH-treated vs. saline-treated rats, suggesting that rapid alterations of synaptic morphology may occur in association with RH. Collectively, these data suggest that RH stress triggers cellular changes that support synaptic plasticity, in specific neuroanatomical sites, which may contribute to the development of hypoglycemia-associated autonomic failure.

Topics: Adrenocorticotropic Hormone; Animals; Blood Glucose; Blotting, Western; Epinephrine; Fluorescent Antibody Technique; gamma-Aminobutyric Acid; Glucagon; Hydrocortisone; Hypoglycemia; Hypothalamus; Hypothalamus, Middle; Immunohistochemistry; Male; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Proto-Oncogene Proteins c-fos; Rats; Rats, Wistar; Recurrence; Synaptophysin; Thyrotropin-Releasing Hormone; Vasopressins

This study used the novel approach of statistical modelling to investigate the control of hypothalamic-pituitary-adrenal (HPA) axis and quantify temporal relationships between hormones. Two experimental paradigms were chosen, insulin-induced hypoglycaemia and 2 h transport, to assess differences in control between noncognitive and cognitive stimuli. Vasopressin and corticotropin-releasing hormone (CRH) were measured in hypophysial portal plasma, and adrenocorticotropin hormone (ACTH) and cortisol in jugular plasma of conscious sheep, and deconvolution analysis was used to calculate secretory rates, before modelling. During hypoglycaemia, the relationship between plasma glucose and vasopressin or CRH was best described by log10 transforming variables (i.e. a positive power-curve relationship). A negative-feedback relationship with log10 cortisol concentration 2 h previously was detected. Analysis of the "transport" stimulus suggested that the strength of the perceived stimulus decreased over time after accounting for cortisol facilitation and negative-feedback. The time course of vasopressin and CRH responses to each stimulus were different However, at the pituitary level, the data suggested that log10 ACTH secretion rate was related to log10 vasopressin and CRH concentrations with very similar regression coefficients and an identical ratio of actions (2.3 : 1) for both stimuli. Similar magnitude negative-feedback effects of log10 cortisol at -110 min (hypoglycaemia) or -40 min (transport) were detected, and both models contained a stimulatory relationship with cortisol at 0 min (facilitation). At adrenal gland level, cortisol secretory rates were related to simultaneously measured untransformed ACTH concentration but the regression coefficient for the hypoglycaemia model was 2.5-fold greater than for transport. No individual sustained maximum cortisol secretion for longer than 20 min during hypoglycaemia and 40 min during transport. These unique models demonstrate that corticosteroid negative-feedback is a significant control mechanism at both the pituitary and hypothalamus. The amplitude of HPA response may be related to stimulus intensity and corticosteroid negative-feedback, while duration depended on feedback alone.

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Animals; Corticotropin-Releasing Hormone; Feedback, Physiological; Female; Hydrocortisone; Hypoglycemia; Hypothalamo-Hypophyseal System; Models, Statistical; Pituitary-Adrenal System; Sheep; Stress, Psychological; Vasopressins

The first objective of this study was to determine whether insulin-induced hypoglycemia (IIH) inhibits LH secretion in unrestrained female macaques during the follicular phase of the menstrual cycle. There was a consistent inhibitory effect of hypoglycemia on LH secretion within 3 h in these females. This inhibition was likely an indirect effect since low glucose levels did not inhibit GnRH secretion from GT1-1 neurones in vitro. We next investigated whether administration of a vasopressin antagonist (AVPa) either alone, or with naloxone could reverse the IIH-induced inhibition of LH release. Females were studied in the follicular phase during 10 h periods with blood samples collected every 10 min. Experimental groups were IIH (n=6), IIH+AVPa (n=5) and IIH+AVPa+naloxone (n=4). The first 5 h of each study served as a control and hypoglycemia was then induced with insulin. The AVPa was given as a bolus (180 microg) just before the insulin and was followed by a continuous infusion (180 microg/h) for 5 h. Naloxone (5 mg/kg) was given with the AVPa and followed by a continuous infusion (5 mg/kg/h) for 5 h. In the IIH group, LH reached its lowest value 3-4 h after insulin. Neither AVPa nor AVPa+naloxone infusion reversed the inhibitory action of hypoglycemia on LH release. These data suggest that if there are inhibitory actions of vasopressin and endogenous opioids on GnRH release induced by hypoglycemia, they are not sufficient to explain the suppression of GnRH/LH release in intact female primates.

Topics: Animals; Arginine Vasopressin; Blood Glucose; Corticotropin-Releasing Hormone; Endorphins; Female; Hydrocortisone; Hypoglycemia; Hypoglycemic Agents; Insulin; Luteinizing Hormone; Macaca mulatta; Menstrual Cycle; Naloxone; Narcotic Antagonists; Vasopressins

Although it is established that the fetus can successfully withstand a single, acute hypoxaemic challenge during gestation, little is known about what effects prevailing adverse intrauterine conditions might have on the fetal response to acute hypoxaemia. The aims of this study were therefore: (1) to characterise the effects of prevailing and sustained hypoxaemia, acidaemia or hypoglycaemia on the fetal cardiovascular responses to an episode of acute hypoxaemia; and (2) to determine the effects of these adverse intrauterine conditions on mechanisms mediating these cardiovascular responses. Thirty-three Welsh Mountain sheep fetuses were chronically instrumented (1-2 % halothane) between 117 and 125 days of gestation (term is ca 145 days) with amniotic and vascular catheters and with a transit-time flow probe around a femoral artery. The animals were divided retrospectively into four groups based upon post-surgical, sustained, basal blood oxygen (chronically hypoxaemic; P(a,O2), 17.3 +/- 0.5 mmHg; n = 8), glucose (chronically hypoglycaemic; blood glucose, 0.49 +/- 0.03 mmol l(-1); n = 6) and acid-base (chronically acidaemic; pH(a), 7.25 +/- 0.01; n = 5) status. Values for compromised fetuses were -2 S.D. from a group of control (n = 14) fetuses. At 130 +/- 4 days, a 1 h episode of acute, isocapnic hypoxaemia (9 % O(2) in N(2), to reduce carotid P(a,O2) to 12 +/- 1 mmHg) was induced in all fetuses by reducing the maternal inspired O(2) fraction (F(I,O2)). Fetal cardiovascular variables were recorded at 1 s intervals throughout the experimental protocol and arterial blood samples taken at appropriate intervals for biophysical (blood gases, glucose, lactate) and endocrine (catecholamines, vasopressin, cortisol, ACTH) measures. During acute hypoxaemia all fetuses elicited hypertension, bradycardia and femoral vasoconstriction. However, prevailing fetal compromise altered the cardiovascular and endocrine responses to a further episode of acute hypoxaemia, including: (1) enhanced pressor and femoral vasoconstriction; (2) greater increments in plasma noradrenaline and vasopressin during hypoxaemia; and (3) basal upward resetting of hypothalamic-pituitary-adrenal axis function. Only chronically hypoxaemic fetuses had significantly elevated basal concentrations of noradrenaline and enhanced chemoreflex function during acute hypoxaemia. These data show that prevailing adverse intrauterine conditions alter the capacity of the fetus to respond to a subsequent episode o

Topics: Acid-Base Equilibrium; Acidosis; Acute Disease; Adrenocorticotropic Hormone; Animals; Blood Gas Analysis; Blood Glucose; Cardiovascular System; Catecholamines; Chemoreceptor Cells; Endocrine System; Female; Fetal Diseases; Fetus; Hemoglobins; Hindlimb; Hydrocortisone; Hydrogen-Ion Concentration; Hypoglycemia; Hypoxia; Lactic Acid; Pregnancy; Sheep; Vascular Resistance; Vasopressins

Lymphocytic hypophysitis is classically defined as an inflammatory disorder confined to adenohypophysis. However, it has recently been indicated that infundibuloneurohypophysitis underlies some subsets of central diabetes insipidus (DI). Therefore, lymphocytic hypophysitis can be considered a syndrome including disorders of both the anterior pituitary (lymphocytic adenohypophysitis) and the posterior pituitary (lymphocytic infundibuloneurohypophysitis). We describe a 77-yr-old woman with lymphocytic hypophysitis presenting with headache, diplopia, general malaise and appetite loss. Head magnetic resonance imaging (MRI) demonstrated pituitary swelling and dura mater thickening on the dorsum sella. Endocrinological investigations revealed both anterior and posterior pituitary dysfunction associated with primary hypothyroidism due to Hashimoto's thyroiditis. Headache and diplopia spontaneously disappeared, and anterior pituitary dysfunction, general malaise and appetite loss improved after taking 10 mg hydrocortisone daily, although ACTH hyposecretion persisted. Pituitary swelling was thereafter reduced but the dura mater thickening persisted. We suggest that this case may represent a variant of lymphocytic hypophysitis in which chronic inflammatory process involves both the anterior and the posterior pituitary gland, infundibulum, dura mater on the dorsum sella and cavernous sinus. Regarding expanding features of lymphocytic hypophysitis, it may be considered a syndrome including heterogeneous disorders, of which the pathogenesis remains to be elucidated.

Topics: Aged; Diplopia; Dura Mater; Female; Hormones; Humans; Hypoglycemia; Insulin; Lymphocytes; Magnetic Resonance Imaging; Pituitary Diseases; Pituitary Hormones; Vasopressins

It is well recognized that the reciprocal interaction established between the immune and neuroendocrine systems is crucial for the homeostatic adaptation of individuals during septicemia. In the present study, using an in vivo rat model, we investigated the degree of participation of central and peripheral epinergic systems in the modulation of the hypothalamic-pituitary-adrenal and immune axes' functions during endotoxemia. For this purpose, acute endotoxemia was induced in adult male rats pretreated intraperitoneally with either different inhibitors of phenylethanolamine-N-methyltransferase (PNMT) [which are active either peripherally (SKF 29661) or both peripherally and centrally (SKF 64139), thus lowering epinephrine (EPI) synthesis] or vehicle only (CTRL). Twelve hours after pretreatment, animals were intraperitoneally injected with vehicle alone (basal) or vehicle containing bacterial lipopolysaccharide (LPS) and sacrificed 2 h later. A significant (p < 0.05 vs. the respective basal value) hypoglycemia was found in all groups studied. No pretreatment modified basal plasma adrenocorticotropic hormone (ACTH), glucocorticoid and cytokine concentrations. Endotoxin-stimulated ACTH secretion was severalfold (p < 0.05) higher than the respective basal value in CTRL and in SKFs-pretreated rats; however, the plasma ACTH levels after LPS were significantly (p < 0.05 vs. CTRL and SKF-29661 values) reduced in SKF-64139-pretreated rats. All groups studied showed an appropriate adrenal response to endotoxin challenge. Although no differences were found in basal anterior pituitary (AP) ACTH content among groups, LPS treatment significantly (p < 0.05 versus the respective basal value) decreased AP ACTH in CTRL and SKF 29661 groups. No pretreatment modified the basal medial basal hypothalamus (MBH) corticotropin-releasing hormone (CRH) content. Conversely, SKF 64139 pretreatment significantly (p < 0.05 vs. CTRL and SKF 29661 values) reduced basal median eminence (ME) CRH content, and LPS administration significantly (p < 0.05) decreased ME CRH in CTRL and SKF-29661-pretreated rats. SKF 64139 pretreatment significantly (p < 0.05) enhanced basal MBH and ME arginine vasopressin (AVP) contents. LPS administration significantly (p < 0.05) decreased MBH AVP in CTRL and SKF-29661-pretreated rats and diminished (p < 0.05 vs. basal values) ME AVP in all groups. The plasma tumor necrosis factor alpha (TNFalpha) concentrations were enhanced severalfold (p < 0.05 vs. basal valu

Topics: Acute-Phase Reaction; Adrenocorticotropic Hormone; Animals; Corticotropin-Releasing Hormone; Enzyme Inhibitors; Epinephrine; Hypoglycemia; Hypothalamo-Hypophyseal System; Isoquinolines; Lipopolysaccharides; Male; Neuroimmunomodulation; Norepinephrine; Phenylethanolamine N-Methyltransferase; Pituitary-Adrenal System; Rats; Rats, Inbred F344; Tetrahydroisoquinolines; Tumor Necrosis Factor-alpha; Vasopressins

Insulin-induced hypoglycaemic (IIH) stress evokes the release of arginine vasopressin (AVP) and suppresses luteinising hormone (LH) pulses in a number of species, a phenomenon augmented by the presence of oestradiol (E2). The aim of this study was to test the hypothesis that AVP not only disrupts pulsatile LH secretion in the female rat, but specifically mediates the effect of IIH stress on suppressing LH release. The role of E2 in augmenting the disruptive effect of AVP on LH secretion was also addressed. Rats were ovariectomized (OVX) and fitted with intracerebroventricular (i.c.v. ) and intravenous (i.v.) cannulae. For experiments requiring comparisons of neuroendocrine responses in the presence and absence of E2, animals were implanted subcutaneously with E2 or oil-filled capsules respectively. AVP (5 microg) administered via the i.c.v. cannula suppressed LH secretion by decreasing LH pulse amplitude without affecting LH pulse frequency, an effect that was blocked by central administration of an AVP antagonist (25 microg). This inhibitory response was evident only in E2-replaced OVX rats, thus suggesting a sensitizing influence of the gonadal steroid. In the AVP-deficient Brattleboro rats, IIH stress did not interrupt pulsatile LH secretion as demonstrated in Long Evans and Wistar controls. While these data might suggest a pivotal role for AVP in stress-induced suppression of LH release, central administration of an AVP antagonist did not prevent the interruption of LH pulses in response to IIH stress. Furthermore, it would appear that AVP is not primarily involved in hypoglycaemic stress-induced suppression of pulsatile LH secretion since central administration of very high doses of AVP resulted in a suppression of LH pulse amplitude and not frequency, while hypoglycaemic stress caused an interruption of LH pulses.

Topics: Animals; Arginine Vasopressin; Estradiol; Female; Hypoglycemia; Hypoglycemic Agents; Insulin; Luteinizing Hormone; Ovariectomy; Pulsatile Flow; Rats; Rats, Brattleboro; Rats, Wistar; Stress, Physiological; Vasopressins

Lewis rats display hyporesponsive hypothalamo-pituitary-adrenocortical (HPA) axes, overproduction of cytokines, and susceptibility to inflammatory disease. The Lewis corticotropin-releasing hormone (CRH) neurosecretory system contains normal numbers of vasopressin (VP)-deficient axon varicosities, but abnormally sparse VP-containing varicosities in the external zone of the median eminence, compared to the normoresponsive Sprague Dawley (SD), Wistar and Fischer 344 strains. Since VP may act as a thyrotropin-releasing factor, we hypothesized that thyroid axis responsivity may be altered in Lewis rats. T3, T4 and TSH were measured by radioimmunoassay, and free T4 by equilibrium dialysis, in adult male Lewis and SD rats. One h cold (5 degrees C) induced significant increases in T3, T4 and TSH levels in Lewis rats but not in SD rats. Ninety min insulin-induced hypoglycemia (1 IU/kg, i.p.) induced a significant T3 increase in Lewis rats and a significant T4 increase in SD rats. Two h after ip LPS (0.25 or 0.75 mg/kg), T4 levels fell significantly in Lewis rats but not in SD rats. TSH decreases were significant in Lewis rats after 0.75 mg/kg and in SD rats after 0.25 mg/kg. Baseline hormone levels were generally higher in Lewis rats; the differences were significant for T3 and T4 in the insulin experiments and for T3, T4 and free T4 in the LPS experiments. The data suggest that reduced inhibition from the adrenocortical axis in Lewis rats leads to hyperresponsivity of the thyroid axis to cold, and greater LPS-induced decreases in T4 levels, probably due to an exaggerated inhibitory cytokine response.

Topics: Adrenal Cortex; Adrenocorticotropic Hormone; Animals; Axons; Blood Glucose; Cold Temperature; Corticotropin-Releasing Hormone; Dose-Response Relationship, Drug; Fasting; Hypoglycemia; Hypoglycemic Agents; Hypothalamo-Hypophyseal System; Insulin; Lipopolysaccharides; Male; Mutation; Neurosecretory Systems; Pituitary Gland; Pituitary-Adrenal System; Rats; Rats, Inbred Lew; Rats, Sprague-Dawley; Thyroid Gland; Thyrotropin; Thyroxine; Triiodothyronine; Vasopressins

Insulin-induced hypoglycemia (IIH) profoundly inhibits the activity of the hypothalamic GnRH pulse generator. The aim of this study was to determine the role of vasopressin and CRF in this response. Ovariectomized rhesus monkeys with chronically implanted recording electrodes in the mediobasal hypothalamus and with intracerebroventricular (icv) cannulas in the lateral ventricle were placed in primate chairs, and blood samples were taken every 10 min. Pulse generator activity was monitored electrophysiologically by detecting characteristic increases in hypothalamic multi-unit activity (MUA volleys) and by attendant LH pulses measured in peripheral blood. Arginine vasopressin (AVP) infused via the i.c.v. cannula (50 micrograms/60 microliters.h) in eight monkeys failed to decrease pulse generator activity, as measured by the frequency of MUA volleys, but decreased mean serum LH concentrations (P < 0.001) while increasing serum cortisol levels (P < 0.02). Central administration of an AVP antagonist ([deamino-Pen1, O-Me-Tyr2-Arg8] vasopressin) in four monkeys at a rate (180 micrograms/60 microliters.h) that had previously been found to block the aforementioned effects of coadministered AVP failed to prevent the IIH-induced inhibition of GnRH pulse generator activity and LH secretion in the same animals. On the other hand, a CRF antagonist, [D-Phe12,Nle21,38,C alpha MeLeu37] rat CRF-(12-41), infused i.c.v. at a rate of 500 micrograms/60 microliters.h in four monkeys, delayed the inhibition of pulse generator frequency in response to IIH. These results suggest that AVP does not mediate the hypoglycemia-induced inhibition of GnRH pulse generator frequency in the rhesus monkey, but that CRF may be involved in this response.

Topics: Animals; Arginine Vasopressin; Cerebral Ventricles; Corticotropin-Releasing Hormone; Electrodes; Electrophysiology; Female; Gonadotropin-Releasing Hormone; Hydrocortisone; Hypoglycemia; Hypothalamus, Middle; Insulin; Luteinizing Hormone; Macaca mulatta; Ovariectomy; Rats; Vasopressins

There is now considerable evidence that nitric oxide is an important neuroregulatory agent, but there has been very little investigation of its possible role in neuroendocrine mechanisms in humans. We have investigated the effects of two nitric oxide precursors, L-arginine and molsidomine, under basal conditions on the pituitary hormones growth hormone (GH), prolactin, luteinizing hormone, follicle-stimulating hormone, thyrotrophin, adrenocorticotrophin (ACTH) and vasopressin, and also on serum cortisol; we have also studied the effect of L-arginine on circulating prolactin, ACTH and cortisol in normal human subjects under hypoglycaemic stress. L-Arginine stimulated both GH and prolactin release under basal conditions but had no effect on the other hormones studied, while the nitric oxide donor molsidomine showed no effect on any hormone studied. L-Arginine potentiated the hypoglycaemia-stimulated release of ACTH but did not influence the rise in GH. The current studies suggest that the effects of L-arginine on the stimulation of GH and prolactin release are unlikely to be mediated via the generation of nitric oxide.

Topics: Adrenocorticotropic Hormone; Adult; Arginine; Blood Glucose; Drug Synergism; Human Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Insulin; Male; Molsidomine; Neurosecretory Systems; Nitric Oxide; Vasodilator Agents; Vasopressins

The objective of the present study was to examine the role of vasopressin in the regulation of LH secretion in the rhesus monkey. The effect of vasopressin administration on basal LH secretion and vasopressin antagonism on stress-induced inhibition of LH secretion were examined. Intracerebroventricular (i.c.v.) infusion of vasopressin (20 micrograms/h) to chair restrained ovariectomized rhesus monkeys (n = 5) decreased the area under the LH curve by -51.61 +/- 13.73 ng/ml/h compared to -8.35 +/- 7.11 ng/ml/h following infusion of artificial CSF (aCSF; p = 0.021). This effect was independent of any change in mean arterial pressure. Subsequently, the role of vasopressin in hypoglycemia-induced suppression of LH was examined. Administration of insulin (1 U/kg BW) to chair-restrained ovariectomized rhesus monkeys decreased the area under the LH curve by -60.88 +/- 19.77 ng/ml/h. The decrease in LH was significantly different from that observed in aCSF-infused euglycemic controls which exhibited a slight decrease in LH (-8.35 +/- 7.11 ng/ml/h; p = 0.036). In contrast, the area under the LH curve was increased slightly (1.42 +/- 11.93 ng/ml/h) when insulin administration was combined with i.c.v. infusion of the vasopressin antagonist [deaminopenicillamine1, O-methyl-tyrosine2, arginine8]-vasopressin (120 micrograms/h; p = 0.013 vs. insulin only). The demonstration that vasopressin administration inhibits LH secretion whereas vasopressin antagonism prevents hypoglycemia-induced LH suppression suggests that vasopressin is a physiological inhibitor of LH secretion in the rhesus monkey.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Cerebrospinal Fluid; Female; Hypoglycemia; Insulin; Luteinizing Hormone; Macaca mulatta; Ovariectomy; Vasopressins

In this study, we examined the effect of passive immunization of endogenous corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) on hypoglycemia-induced adrenocorticotropic hormone (ACTH) secretion and determined proopiomelanocortin messenger RNA (POMC mRNA) levels in the anterior pituitary as well as hypothalamic CRF mRNA levels in pentobarbital anesthetized rats. The response of plasma ACTH to hypoglycemia was partially inhibited by the administration of CRF-antiserum (CRF-As) or AVP-antiserum (AVP-As) alone, but was found to be completely abolished by the administration of CRF-As + AVP-As as compared to the response in normal rabbit serum-treated rats. The hypoglycemia-induced POMC mRNA level in the anterior pituitary was completely inhibited by the administration of CRF-As alone and CRF-As + AVP-As, but was not inhibited by AVP-As alone as compared to the response in normal rabbit serum-treated rats. The administration of CRF-As and/or AVP-As did not affect hypoglycemia-induced CRF mRNA levels in the hypothalamus. These results indicate that the synergistic effect of CRF and AVP is important for hypoglycemia-induced ACTH secretion, but CRF is essential and indispensable for hypoglycemia-induced POMC gene expression in the anterior pituitary (AP).

Topics: Animals; Arginine Vasopressin; Blood Glucose; Blotting, Northern; Corticotropin-Releasing Hormone; Hypoglycemia; Hypothalamus; Immunoglobulin G; Male; Pituitary Gland, Anterior; Pro-Opiomelanocortin; Radioimmunoassay; Rats; Rats, Inbred Strains; RNA, Messenger; Vasopressins

Factors from the neurohypophysis are important in the control of anterior pituitary function. This study evaluated the hypothesis that the neurophypophysis is an integral component of the adrenocorticotropin (ACTH) response to certain stimuli. Furthermore, we investigated the possibility that the importance of the neurohypophysis during corticotropic stimuli can be classified by the magnitude of the systemic vasopressin response induced. The ACTH response to insulin-induced hypoglycemia (INS), nitroprusside hypotension (NP), or ovine corticotropin-releasing factor (CRF) infusion (20 ng/kg/min) was measured in dogs before (intact) and greater than 2 weeks after selective transbuccal neurohypophysectomy (NHX). INS (0.2 U/kg) resulted in a significant decrease in plasma glucose from 93 +/- 1 to 33 +/- 2 mg/dl at 30 min and a significant increase in plasma ACTH from 53 +/- 10 to 306 +/- 33 pg/ml in intact dogs whereas the vasopressin (AVP) response was small (2.8 +/- 0.3 to 5.5 +/- 0.7 pg/ml). NHX had no effect on the blood glucose or ACTH response to INS. NP resulted in large increases in ACTH from 54 +/- 8 to 351 +/- 89 pg/ml and in AVP from 2.7 +/- 0.2 to 272 +/- 98 pg/ml. In contrast to INS, NHX significantly attenuated the ACTH and AVP responses to NP. The ACTH response to CRF was not attenuated by NHX, indicating normal pituitary corticotropic function. In summary, NHX attenuated the ACTH response to hypotension (large peripheral AVP response) but not to INS or CRF (small peripheral AVP response).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenocorticotropic Hormone; Animals; Blood; Blood Glucose; Corticotropin-Releasing Hormone; Dogs; Hydrocortisone; Hypoglycemia; Hypophysectomy; Hypotension; Insulin; Male; Nitroprusside; Osmolar Concentration; Potassium; Sodium; Vasopressins

A functional ultrastructural assay was used to determine the response of corticotropin releasing hormone (CRH) neurosecretory cells to short-term stress. Depletion of neurosecretory vesicles from axonal swellings in the external zone of the rat median eminence was used as a measure of functional activity. One hour of immobilization or 5 h of insulin-induced hypoglycemia caused marked depletion of vesicles from the vasopressin (VP)-containing CRH axons, but had no effect on the VP-deficient subpopulation of CRH axons. Injection of colchicine (100 micrograms) into the lateral ventricle also resulted in selective depletion of vesicles from the VP-containing subpopulation over the course of 5 h, with no depletion from the VP-deficient axons. By 24 h after injection of 100 micrograms colchicine, however, both the VP-containing and the VP-deficient axons were severely depleted of neurosecretory vesicles. These data demonstrate for the first time that the CRH neurosecretory system contains functionally distinct components, and that the VP secreting component may specifically mediate the ACTH response to short-term stress.

Topics: Animals; Axons; Colchicine; Corticotropin-Releasing Hormone; Cytoplasmic Granules; Hypoglycemia; Insulin; Male; Median Eminence; Neurons; Rats; Restraint, Physical; Stress, Physiological; Vasopressins

Insulin hypoglycaemia causes a rise in plasma vasopressin concentrations in man and the rat, and vasopressin stimulates glucagon secretion and increases hepatic glucose output in man. Vasopressin has also been suggested to have an important synergistic role with corticotrophin releasing factor in the release of adrenocorticotrophin hormone, and a counter-regulatory role for the hormone has been proposed. As diminished anterior pituitary hormone responses to hypoglycaemia have been reported in diabetes mellitus, we studied the plasma vasopressin responses to insulin-induced hypoglycaemia in 10 patients with established Type 1 diabetes and 10 matched control subjects. Blood glucose fell from 4.5 +/- 0.3 to 1.6 +/- 0.1 mmol l-1 (p less than 0.001) in the diabetic group and from 4.6 +/- 0.2 to 1.5 +/- 0.2 mmol l-1 (p less than 0.001) in control subjects, with delayed blood glucose recovery in the diabetic patients. Plasma vasopressin rose in the diabetic patients from 0.9 +/- 0.2 to 6.9 +/- 2.8 pmol l-1 (p less than 0.001), a significantly greater rise (p less than 0.05) than in the control subjects, 0.8 +/- 0.1 to 2.4 +/- 1.0 pmol l-1 (p less than 0.001). Plasma osmolalities remained unchanged and haemodynamic changes were similar in both groups. There is an exaggerated rise in plasma vasopressin concentrations in diabetic patients in response to insulin-induced hypoglycaemia. The putative mechanisms and potential significance of the exaggerated rise are discussed.

Topics: Adult; Blood Pressure; Diabetes Mellitus, Type 1; Growth Hormone; Hematocrit; Humans; Hydrocortisone; Hypoglycemia; Insulin; Kinetics; Pulse; Reference Values; Vasopressins

To study possible adrenergic modulation of pituitary-adrenal responses to insulin-induced hypoglycemia and CRH we examined the effect of nonselective alpha-blockade (phentolamine) and nonselective beta-blockade (propranolol) on plasma ACTH, cortisol, and vasopressin (AVP) responses to hypoglycemia and CRH in five normal men. Infusion of propranolol or phentolamine did not alter basal plasma ACTH or cortisol levels. The propranolol infusion enhanced the stimulatory effect of hypoglycemia on ACTH, cortisol, and AVP secretion and also enhanced the stimulatory effect of CRH on ACTH and cortisol secretion. Infusion of phentolamine inhibited hypoglycemia-induced ACTH and AVP secretion, but had no effect on the stimulatory effect of CRH on ACTH and cortisol secretion. The increments of plasma ACTH and cortisol induced by an almost maximal dose of CRH (1 microgram/kg) were smaller than those induced by hypoglycemia. The propranolol-induced enhancement of the ACTH response to hypoglycemia was almost the same as the ACTH response to CRH alone. From these results we conclude that propranolol may act at the pituitary level to enhance CRH action, rather than AVP action, and that the ACTH response to hypoglycemia may be mediated by hypothalamic alpha-adrenergic activation.

Topics: Adrenocorticotropic Hormone; Blood Glucose; Corticotropin-Releasing Hormone; Female; Hemodynamics; Humans; Hydrocortisone; Hypoglycemia; Insulin; Phentolamine; Propranolol; Vasopressins

Insulin administration to overnight fasted rats causes a dose-dependent decline in plasma glucose concentrations and a dose-dependent increase in plasma ACTH concentrations. The ACTH response, but not the glucose response, was blocked by treatment with chlorpromazine-morphine-pentobarbital, indicating that the main factors triggering the ACTH response are of central, rather than peripheral, origin. To study whether insulin affected the turnover of CRF and vasopressin (AVP) in the zona externa of the median eminence (ZEME), we determined the rate of decline of both hypophysiotropic factors in rats with or without blockade of axonal transport by colchicine. In the ZEME, the concentrations of CRF and AVP were assessed by quantitative immunocytochemistry (QICC) in tissue sections or by RIA in median eminence extracts. QICC allows selective quantification of AVP and other peptides within the ZEME. The changes in the CRF content, as measured by QICC and RIA, were linearly correlated (r = 0.99), demonstrating that changes in peptide-staining intensity reflect changes in peptide content. Colchicine, when given intracisternally in a nontoxic dose of 5 micrograms, had no marked effect on resting plasma levels of ACTH and only slightly reduced the ACTH response to insulin-induced hypoglycemia. In the ZEME, CRF and AVP concentrations at rest were not affected by colchicine. In colchicine-treated rats insulin-induced hypoglycemia resulted in a prominent decline in CRF and AVP concentrations in the ZEME. The CRF concentration declined at a rate of 23%/h over a period of 3 h. The AVP concentration declined to a similar extent as CRF over the first hour, but tended to fall at the later time points. We conclude that hypoglycemia increases turnover of both CRF and AVP in the ZEME. However, the turnover rates of both hypophysiotropic peptides do not appear to be quantitatively coupled.

Topics: Adrenocorticotropic Hormone; Animals; Blood Glucose; Colchicine; Corticosterone; Corticotropin-Releasing Hormone; Hypoglycemia; Immunohistochemistry; Insulin; Male; Median Eminence; Radioimmunoassay; Rats; Rats, Inbred Strains; Vasopressins

The diabetes insipidus which accompanies the DIDMOAD (Wolfram) syndrome is thought to be hypothalamic in origin, though no formal study of vasopressin secretion in the syndrome has been published, and some data in the literature suggest a renal tubular defect. We have studied vasopressin secretion in seven patients with the Wolfram/DIDMOAD syndrome during three dynamic stimuli: an osmotic stimulus (hypertonic saline infusion), hypoglycaemia (insulin tolerance test) and a baroregulatory stimulus (trimetaphan infusion). Hypertonic saline infusion demonstrated three patients to have complete and four to have partial hypothalamic diabetes insipidus; administration of (per nasal) desmopressin excluded nephrogenic diabetes insipidus in all seven patients. Insulin hypoglycaemia failed to stimulate vasopressin release, but trimetaphan-induced hypotension produced significant though subnormal rises in plasma vasopressin in three patients with partial diabetes insipidus, though it produced a negligible rise and no rise in plasma vasopressin in two patients with complete diabetes insipidus. The data suggest a much greater frequency of hypothalamic diabetes insipidus in the Wolfram/DIDMOAD syndrome than is reported, but did not identify nephrogenic diabetes insipidus. The absence of vasopressin responses to non-osmotic stimuli in patients with complete diabetes insipidus suggests global lack of vasopressin secreting neurones, rather than an isolated osmoreceptor defect or selective vasopressin secreting neuronal loss, as the lesion producing diabetes insipidus in the DIDMOAD syndrome.

Topics: Adult; Blood Glucose; Blood Pressure; Female; Humans; Hypoglycemia; Infusions, Parenteral; Insulin; Male; Osmolar Concentration; Saline Solution, Hypertonic; Trimethaphan; Vasopressins; Wolfram Syndrome

Body temperature falls during hypoglycaemia, perhaps as a protective mechanism. To test the hypothesis that the skin blood flow response to hypoglycaemia is specifically designed to facilitate heat loss we studied both nutritional blood flow and arteriovenous shunting of blood in skin during prolonged, controlled hypoglycaemia in man. We studied eight otherwise healthy, male, Type 1 (insulin-dependent) diabetic patients. Under Biostator control blood glucose was clamped at 8.0 (7.9-8.9), mmol/l (median and range) for 30 min, reduced to symptomatic hypoglycaemia, 1.7 (1.0-2.6) mmol/l for 20 min then raised to 4.9 (3.3-6.7) mmol/l. Interdigital skin web blood flow (laser doppler flowmeter, nutritional flow) fell during hypoglycaemia from 3.1 (2.2-3.8) to 2.4 (1.2-2.8) volts and remained depressed. In contrast, finger blood flow (venous occlusion plethysmography, arteriovenous shunt flow) started high at 54.7 (17.4-85.6), remained high at 52.7 (38.1-81.4) during hypoglycaemia but fell sharply to 25.3 (4.2-66.2) ml.min-1.100 ml-1 when symptoms were relieved. Plasma adrenaline and vasopressin both rose during hypoglycaemia from 0.4 (0.05-0.8) to 4.5 (2.3-20.2) nmol/l and from 0.5 (0.5-3.5) to 4.4 (2.0-13.9) pg/ml, respectively, and both fell sharply thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Blood Glucose; Body Temperature; Diabetes Mellitus, Type 1; Epinephrine; Face; Fingers; Forearm; Heart Rate; Humans; Hypoglycemia; Insulin; Insulin, Regular, Pork; Male; Regional Blood Flow; Skin; Vasopressins

We studied the influence of a hypertonic saline infusion on the counterregulatory response to insulin-induced hypoglycemia in nine normal men. When given hypertonic saline, the men had less hypoglycemia in response to insulin, both acutely and in the recovery phase (P less than 0.01), and released 34% more glucagon (P less than 0.05) than when they were water loaded. The total integrated ACTH, cortisol, epinephrine, norepinephrine, and GH responses to hypoglycemia were similar after saline and water loading. After the saline load, the mean plasma vasopressin level rose from 11.0 +/- 2.2 (+/- SEM) to 20.9 +/- 2.9 pg/mL in response to insulin-induced hypoglycemia. In contrast, after the water load, vasopressin levels were undetectable (less than 2 pg/mL) and they increased only to 2.6 +/- 0.4 pg/mL with hypoglycemia. There was a significant positive correlation between basal plasma vasopressin and nadir glucose concentrations and a significant negative correlation between basal plasma vasopressin and the integrated fall in glucose after insulin administration (P less than 0.01 and P less than 0.025, respectively). The difference in the glycemic response to insulin may be related to the high vasopressin levels after saline loading, which could, either directly and/or through enhanced glucagon release, increase hepatic glucose production and thus limit the hypoglycemic response to insulin.

Topics: Adrenocorticotropic Hormone; Adult; Catecholamines; Glucagon; Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Insulin; Male; Saline Solution, Hypertonic; Sodium Chloride; Vasopressins

Topics: Epinephrine; Factor VIII; Hemostasis; Humans; Hypoglycemia; Vasopressins

Factor VIII (FVIII) and plasminogen activator activity (PAA) rise during hypoglycaemia, and this might contribute to the vascular complications of diabetes. Similar changes in haemostasis accompany raised plasma levels of vasopressin (aVP) and adrenaline. To investigate the effects of these hormones on haemostasis during hypoglycaemia and the role of plasma insulin concentrations, eight insulin-dependent diabetic patients underwent controlled hypoglycaemia for 20 min and 13 diabetic patients were investigated during hyperinsulinaemia with blood glucose maintained at 8.0 mmol/l. During hypoglycaemia, insulin levels increased to median values of 114 mU/l, a VP rose from 0.5 to 4.4 (p less than 0.005) pg/ml and adrenaline from 0.4 to 4.4 nmol/l (p less than 0.005). FVIII coagulant activity (FVIII:C) rose from 0.75 to 1.09 IU/ml (p less than 0.01) and the ristocetin co-factor (FVIIIR:Co) and von Willebrand factor antigen (vWF:Ag) showed similar responses. PAA increased from 156 to 745 units (p less than 0.005). During hyperinsulinaemia, insulin rose following infusion from 24 to 52 and 118 mU/l, maintained for an hour at each level. Despite this, plasma aVP, FVIII:C, FVIIIR:Co, vWF:Ag and PAA remained unchanged. This study indicates that the marked changes in FVIII, vWF and PAA concentrations which accompany hypoglycaemia depend on low blood glucose and not raised plasma insulin. The response in probably mediated by increases in adrenaline and aVP, which are part of the physiological response to hypoglycaemia.

Topics: Adolescent; Adult; Antigens; Diabetes Mellitus, Type 1; Epinephrine; Factor VIII; Hemostasis; Hormones; Humans; Hypoglycemia; Insulin; Male; Middle Aged; Plasminogen Activators; Vasopressins; von Willebrand Factor

The hypophysiotropic coding of ACTH secretion resulting from insulin-induced hypoglycemia was investigated in urethane-anesthetized fasted rats. The participation of corticotropin-releasing factor (CRF), arginine vasopressin (AVP), and catecholamines in the ACTH response was first investigated by systemic administration of CRF antiserum, an AVP pressor antagonist, or a ganglionic blocking agent. These treatments were without effect on the hypoglycemic response, which was characterized by a 67% fall in systemic glucose levels within 30 min of insulin administration. ACTH secretion in response to insulin-induced hypoglycemia was differentially affected by these pharmacological treatments. Administration of antiserum to CRF abolished the ACTH response, whereas ganglionic blockade was without significant effect. However, administration of a vasopressinergic pressor antagonist significantly attenuated ACTH secretion after insulin treatment. These observations suggested the participation of both CRF and AVP in mediation of the ACTH secretory response to hypoglycemia. Infusion of glucose to counter the hypoglycemia action of insulin injection prevented the ACTH secretory response. Measurement of immunoreactive (ir) CRF, irAVP, and ir-oxytocin in sequential collections of hypophysial portal plasma revealed a significant elevation of irAVP concentration without concomitant elevation of irCRF or ir-oxytocin levels. We propose that CRF functions in a permissive role, maintaining a relatively constant portal concentration and thereby allowing expression of the weaker ACTH-releasing activity of AVP and other secretagogues. Thus, AVP, not CRF, appears to represent the dynamic mediator of ACTH secretion accompanying insulin-induced hypoglycemia. These observations provide additional support for the hypothesis of multifactor stimulus-specific hypophysiotropic coding of ACTH secretion.

Topics: Adrenocorticotropic Hormone; Animals; Arginine Vasopressin; Catecholamines; Chlorisondamine; Corticotropin-Releasing Hormone; Hypoglycemia; Hypothalamus; Immune Sera; Insulin; Male; Pituitary Gland; Rats; Rats, Inbred Strains; Vasopressins

Sixteen children had congenital optic nerve hypoplasia and hypothalamic-pituitary dysplasia. Investigation disclosed an extremely variable spectrum of neuroendocrinological findings that ranged from deficiency to hypersecretion of trophic hormone. Neuroendocrine abnormalities consisted mainly of trophic hormone deficiencies, the most common being growth hormone deficiency, but trophic hormone hypersecretion, including growth hormone, corticotropin, and prolactin was found as well. The extent of anterior pituitary hormone deficiency was variable. Anti-diuretic hormone deficiency was presented in two patients. Our findings support the concept of hypothalamic defect as the major cause for the pituitary dysfunction in this syndrome. Physicians should be aware of this syndrome as a common cause for growth failure and multiple pituitary hormone deficiencies in visually impaired children, which would facilitate the diagnosis and early institution of therapy for this treatable but potentially serious entity.

Topics: Adolescent; Adult; Brain; Child; Child, Preschool; Female; Gonads; Growth Hormone; Humans; Hypoglycemia; Hypopituitarism; Hypothalamo-Hypophyseal System; Infant; Male; Optic Nerve; Pituitary-Adrenal System; Pneumoencephalography; Prolactin; Thyroid Gland; Tomography, X-Ray Computed; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Blood Glucose; Carotid Arteries; Dogs; Epinephrine; Female; Hematocrit; Hypoglycemia; Insulin; Male; Osmolar Concentration; Sodium; Vasopressins

Topics: Adrenocorticotropic Hormone; beta-Lipotropin; Calcitonin; Chorionic Gonadotropin; Corticotropin-Releasing Hormone; Growth Hormone; Growth Hormone-Releasing Hormone; Hormones, Ectopic; Humans; Hypercalcemia; Hypoglycemia; Paraneoplastic Endocrine Syndromes; Parathyroid Hormone; Vasopressins

Topics: Arginine Vasopressin; Body Water; Deamino Arginine Vasopressin; Diabetes Insipidus; Humans; Hypernatremia; Hypoglycemia; Hyponatremia; Inappropriate ADH Syndrome; Pharmacology; Radioimmunoassay; Vasopressins; Water-Electrolyte Imbalance

A 36-yr-old woman with a chronic wasting illness associated with hyponatremia and hypotension proved to have secondary adrenal insufficiency and low levels of GH and PRL. TSH, LH, and FSH responses remained normal. Aldosterone excretion was markedly reduced (0.74 microgram/day) before replacement therapy was started, but normal renin and aldosterone responses to sodium restriction were observed after 6 months of corticosteroid treatment. These responses were maintained after acute steroid withdrawal despite the continued absence of ACTH. Chronically adequate glucocorticoid levels were necessary to maintain a normal aldosterone response in this patient. If there is also a pituitary factor required for this response, it does not appear to be ACTH.

Topics: Adrenocorticotropic Hormone; Adult; Aldosterone; Blood Glucose; Dexamethasone; Female; Fludrocortisone; Follicle Stimulating Hormone; Growth Hormone; Humans; Hypoglycemia; Hyponatremia; Insulin; Luteinizing Hormone; Prolactin; Sodium; Thyrotropin; Vasopressins

4 patients with presumed pituitary hypothalamic sarcoidosis are described. 3 had histological diagnoses compatible with sarcoidosis and in the other this diagnosis was strongly suspected from chest X-rays. 2 patients presented with diabetes insipidus. ACTH reserve was diminished in 3 out of 4 and growth hormone reserve was diminished in the 3 who were tested. All 4 patients developed secondary amenorrhea. 3 patients had hypothalamic hypothyroidism. Prolactin dynamics were intact. Tomograms of the sella turcica in all 4 and computerized tomography of the hypothalamic area in 2 patients failed to reveal any abnormality.

Topics: 17-Hydroxycorticosteroids; Adolescent; Adrenocorticotropic Hormone; Adult; Female; Gonadotropin-Releasing Hormone; Growth Hormone; Humans; Hydrocortisone; Hydroxysteroids; Hypoglycemia; Hypopituitarism; Hypothalamo-Hypophyseal System; Insulin; Luteinizing Hormone; Metyrapone; Middle Aged; Prolactin; Sarcoidosis; Thyrotropin; Thyrotropin-Releasing Hormone; Vasopressins

Topics: Adrenocorticotropic Hormone; Cushing Syndrome; Erythropoietin; Gonadotropins; Hormones, Ectopic; Humans; Hypercalcemia; Hypoglycemia; Hyponatremia; Insulin; Melanocyte-Stimulating Hormones; Paraneoplastic Endocrine Syndromes; Parathyroid Hormone; Pigmentation Disorders; Vasopressins

Insulin-induced hypoglycaemia caused a threefold rise in plasma-arginine-vasopressin concentration (to 4-36 +/- 0-77 pmol/1) in ten subjects who had normal posterior-pituitary function. Plasma-arginine vasopressin reached a peak 30 min after injection of insulin. Plasma concentrations of arginine vasopressin obtained with hypoglycaemia were similar to those achieved after overnight dehydration for 14-16 h. No rise in plasma-arginine-vasopressin was observed in three patients with cranial diabetes insipidus in whom severe hypoglycaemia developed after insulin infusion. It is suggested that the measurement of arginine vasopressin during insulin-induced hypoglycaemia may be a useful clinical test of posterior-pituitary function.

Topics: Adolescent; Adult; Arginine Vasopressin; Blood Glucose; Diabetes Insipidus; Female; Humans; Hypoglycemia; Injections, Intravenous; Insulin; Male; Middle Aged; Pituitary Function Tests; Pituitary Gland, Posterior; Time Factors; Vasopressins

The response of plasma ACTH and/or cortisol concentrations to thyrotropin-releasing-factor (TRF), vasopressin, and insulin administration was determined in 5 patients with Nelson's syndrome and 12 patients with untreated Cushing's disease. TRF administration was associated with a mean increment of 267 pg/ml in plasma ACTH concentrations in patients with Nelson's syndrome, and of 42 pg/ml in patients with Cushing's disease. The increment in plasma cortisol concentrations in the latter group was 12 mug%. No ACTH or cortisol response was observed in normal subjects. Patients with Cushing's disease or Nelson's syndrome exhibited significantly greater increments in plasma ACTH concentrations in response to vasopressin administration (P less than .05, P less than .02 respectively) than did normal subjects; the increment in cortisol concentration was also greater, (P less than .05), in patients with Cushing's disease than in normal subjects. No significant difference was present between patients with Cushing's disease and Nelson's syndrome with regard to the magnitude of the ACTH response to vasopressin administration. In contrast, the increment in plasma cortisol and plasma ACTH concentrations following insulin induced hypoglycemia was significantly less in patients with Cushing's disease than seen in normal subjects, (P less than .001, P less than .05 respectively); while this stimulus was associated with a significantly greater increment in plasma ACTH concentrations in patients with Nelson's syndrome as compared to that seen in normal subjects, (P less than .01) and in patients with Cushing's disease (P less than .01). These findings indicate that pituitary function in patients with Nelson's syndrome is not autonomous and suggest the possibility that altered central nervous regulatory mechanism might play a role in the etiology of the pituitary tumors which are frequently associated with this syndrome. The TRF induced rise in plasm cortisol and ACTH concentrations in patients with Cushing's disease and Nelson's syndrome suggests the possibility of altered hypothalamic or pituitary receptors in such patients.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Female; Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Insulin; Klinefelter Syndrome; Male; Middle Aged; Prolactin; Thyrotropin; Thyrotropin-Releasing Hormone; Vasopressins

Topics: Adrenocorticotropic Hormone; Humans; Hypoglycemia; Insulin; Lysine; Metyrapone; Pituitary-Adrenal Function Tests; Vasopressins

The effect of metergoline, a specific antiserotoninergic drug, on ACTH secretion was investigated in 29 normal volunteers and in 4 patients with increased ACTH production (3 with Addison's disease, 1 with Cushing's disease). In 15 normal subjects, a 4-day treatment with 10 mg daily of metergoline significantly blunted the ACTH response to insulin hypoglycemia. Mean peak ACTH values before and after treatment were, respectively, 333 +/- 39.2 (SE) and 235 +/- 38.8 pg/ml (P less than 0.05). The corresponding values of plasma cortisol were 29.6 +/- 2.96 and 20.5 +/- 2.67 mug/100 ml (P less than 0.05). In contrast, metergoline failed to affect the ACTH response to lysine-vasopressin (LVP) administered iv (8 subjects studied) and im (6 subjects studied). In 3 patients suffering from Addison's disease, an appreciable although not statistically significant lowering of the plasma ACTH levels was noted during metergoline administration. The mean pre- and post-treatment values of plasma ACTH in these patients were, respectively, 1116 +/- 192.2 and 666 +/- 100.8 pg/ml, 4240 +/- 50.0 and 3398 +/- 368.0 pg/ml, and 431 +/- 44.0 and 352 +/- 23.9 pg/ml. In one patient with Cushing's disease caused by a pituitary adenoma, metergoline did not appreciably modify plasma ACTH levels. Taken together, these results lend support to the concept of a physiological stimulating effect of serotonin on ACTH secretion. Moreover, they are compatible with the view that serotonin exerts its action chiefly at the hypothalamic level while LVP promotes ACTH release by a primary action on the pituitary.

Topics: Addison Disease; Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Ergolines; Female; Humans; Hydrocortisone; Hypoglycemia; Hypothalamo-Hypophyseal System; Insulin; Lypressin; Male; Metergoline; Middle Aged; Serotonin; Serotonin Antagonists; Vasopressins

Among the malignant tumors of nonendocrine origin that are capable of producing polypeptide hormones and of manifesting as different endocrine syndromes discussed here are ectopic ACTH syndrome, SIADH, and ectopic gonadotropin-producing tumors.

Topics: Adrenocorticotropic Hormone; Carcinoma, Hepatocellular; Carcinoma, Small Cell; Chorionic Gonadotropin; Cushing Syndrome; Diagnosis, Differential; Erythropoietin; Follicle Stimulating Hormone; Gynecomastia; Hormones, Ectopic; Humans; Hyperthyroidism; Hypoglycemia; Hyponatremia; Liver Neoplasms; Lung Neoplasms; Luteinizing Hormone; Male; Paraneoplastic Endocrine Syndromes; Polycythemia; Puberty, Precocious; Thyrotropin; Vasopressins; Water Intoxication

The exact prevalence of the humoral syndromes associated with neoplasm is not known but it seems clear that they exist more commonly than is realized. Hormonal syndromes are very often seen in patients with carcinoma of the lung. Awareness of the large number of ectopic hormonal syndromes in patients with tumors can lead to early diagnosis, treatment, and herald recurrence. They may be responsible for new signs and symptoms which can be life-shortening. Hormonal causes of clinical deterioration must be considered before concluding that symptoms are due to metastases in patients with neoplastic disease. Tumors are chemically active and the important concept which has had great impact on the diagnosis, treatment, and basic understanding of mechanisms, which are important to endocrinologists and oncologists has been stated by Liddle: "Certain tumors of nonendocrine tissue can produce hormones that are similar to normal hormones except that their production is not appropriately controlled by normal physiologic mechanisms." Survival and quality of life can be reduced in patients with the metabolic complications of these humors. The list of humoral substances released by tumors is growing as technologic advances lead to their detection. Other chemical substances produced by neoplastic tissue may have biologic activity which impacts on the patient's clinical condition and which we cannot recognize, at this time, because the techniques to detect them have not been developed. If there are signs or symptoms of overproduction of a hormone, search for a tumor; if a patient has a tumor, search for biologically active substances.

Topics: Cushing Syndrome; Erythropoietin; Hormones; Hormones, Ectopic; Humans; Hypercalcemia; Hypoglycemia; Neoplasms; Paraneoplastic Endocrine Syndromes; Vasopressins

Topics: Adrenocorticotropic Hormone; Adult; Aldosterone; Biological Assay; Circadian Rhythm; Dexamethasone; Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Immunoassay; Insulin; Male; Pituitary Gland; Pituitary-Adrenal Function Tests; Testis; Testosterone; Thyroid Gland; Thyrotropin; Thyrotropin-Releasing Hormone; Triiodothyronine; Trypsin; Vasopressins

Topics: Adrenocorticotropic Hormone; Arginine; Diethylstilbestrol; Dihydroxyphenylalanine; Endotoxins; Female; Glucagon; Glucocorticoids; Glucose; Gonadal Steroid Hormones; Growth Hormone; Humans; Hypoglycemia; Hypothyroidism; Insulin; Male; Obesity; Physical Exertion; Pituitary Function Tests; Pseudomonas; Puberty; Sleep; Vasopressins

Topics: Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Diagnosis, Differential; Female; Follicle Stimulating Hormone; Growth Hormone; Hormones, Ectopic; Humans; Hyperthyroidism; Hypocalcemia; Hypoglycemia; Hyponatremia; Insulin; Luteinizing Hormone; Mediastinal Neoplasms; Middle Aged; Osmolar Concentration; Parathyroid Hormone; Pigmentation Disorders; Syndrome; Thymus Neoplasms; Thyrotropin-Releasing Hormone; Vasopressins

Topics: Administration, Oral; Adrenal Cortex Hormones; Adult; Aged; Arthritis, Rheumatoid; Circadian Rhythm; Cosyntropin; Female; Humans; Hydrocortisone; Hypoglycemia; Hypothalamo-Hypophyseal System; Insulin; Lysine; Male; Metyrapone; Middle Aged; Vasopressins

Topics: 17-Hydroxycorticosteroids; Acromegaly; Adenoma, Chromophobe; Adolescent; Adrenal Glands; Adrenocorticotropic Hormone; Adult; Child; Craniopharyngioma; Dexamethasone; Humans; Hypoglycemia; Hypothalamus; Insulin; Lysine; Metyrapone; Middle Aged; Pituitary Gland; Pituitary Neoplasms; Pituitary-Adrenal Function Tests; Pyrogens; Sella Turcica; Vasopressins

Topics: Adrenal Glands; Adrenal Insufficiency; Blindness; Bradycardia; Brain; Electrolytes; Female; Glucagon; Glucose; Glucose Tolerance Test; Growth Hormone; Humans; Hypoglycemia; Hypopituitarism; Infant; Infant, Newborn; Infant, Newborn, Diseases; Insulin; Intellectual Disability; Male; Pituitary Gland; Seizures; Vasopressins

Topics: Adenocarcinoma; Adenoma; Adrenal Cortex Hormones; Adrenal Gland Neoplasms; Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Arginine; Carbon Isotopes; Cushing Syndrome; Growth Hormone; Humans; Hydroxycorticosteroids; Hypoglycemia; Insulin; Luteinizing Hormone; Lysine; Pituitary Irradiation; Stimulation, Chemical; Vasopressins

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Anthropometry; Arginine; Arm; Body Height; Body Weight; Eunuchism; Gigantism; Glucagon; Gonadotropins; Growth Disorders; Growth Hormone; Humans; Hypoglycemia; Hypopituitarism; Insulin; Male; Pituitary Hormones; Thyrotropin; Vasopressins

Topics: Adolescent; Adult; Blood Glucose; Child; Child, Preschool; Chlorpropamide; Diabetes Insipidus; Drug Synergism; Ethanol; Glyburide; Humans; Hypoglycemia; Metformin; Middle Aged; Osmolar Concentration; Sodium; Thiazines; Vasopressins; Water

Topics: 11-Hydroxycorticosteroids; 17-Hydroxycorticosteroids; Adolescent; Adrenal Glands; Adrenal Insufficiency; Blood Glucose; Child; Child, Preschool; Dwarfism; Evaluation Studies as Topic; Female; Humans; Hypoglycemia; Hypopituitarism; Hypothalamus; Insulin; Lysine; Male; Metyrapone; Obesity; Pituitary Gland; Pituitary-Adrenal Function Tests; Time Factors; Vasopressins

Topics: Adrenal Gland Diseases; Endocrine System Diseases; Erythrocytes; Female; Gastrins; Gynecomastia; Hormones, Ectopic; Humans; Hypercalcemia; Hyperplasia; Hyperthyroidism; Hypoglycemia; Male; Malignant Carcinoid Syndrome; Metabolic Diseases; Neoplasms; Neurologic Manifestations; Polycythemia; Prognosis; Puberty, Precocious; Vasopressins

Topics: Diuretics; Extracellular Space; Humans; Hyperlipidemias; Hypoglycemia; Hyponatremia; Osmolar Concentration; Plasma Volume; Sodium; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Adrenal Glands; Adrenocortical Hyperfunction; Adult; Circadian Rhythm; Cushing Syndrome; Dexamethasone; Electroencephalography; Female; Growth Hormone; Humans; Hydrocortisone; Hydroxycorticosteroids; Hypoglycemia; Hypothalamus; Insulin; Male; Middle Aged; Pituitary Gland; Pituitary-Adrenal Function Tests; Polysaccharides, Bacterial; Sleep Stages; Vasopressins

Topics: Adrenocorticotropic Hormone; Arginine; Chromatography, Paper; Humans; Hydrocortisone; Hypertension; Hypoglycemia; Oxidoreductases; Vasopressins

Topics: Adrenocorticotropic Hormone; Arginine; Growth Hormone; Humans; Hypoglycemia; Insulin; Insulin Secretion; Sympatholytics; Thyrotropin; Vasopressins

Topics: Adult; Clomiphene; Craniocerebral Trauma; Endocrine System Diseases; Estrogens, Conjugated (USP); Humans; Hyperaldosteronism; Hypoglycemia; Hypopituitarism; Insulin; Laurence-Moon Syndrome; Luteinizing Hormone; Male; Puberty, Precocious; Radioimmunoassay; Turner Syndrome; Vasopressins

Ectopic production of polypeptide hormones by tumors of nonendocrine tissues can serve as a clue to diagnosis of the tumor and as a focus for management of the patient with cancer. In the differential diagnosis of syndromes of endocrine hyperfunction, the ectopic hormone syndromes have achieved an increasingly prominent position. Available evidence on the properties of ectopic ACTH, MSH, parathyroid hormone, erythropoietin, gonadotropins, and thyrotropin is consistent with the unifying hypothesis of genetic derepression.

Topics: Abdominal Neoplasms; Adenocarcinoma; Adrenocortical Hyperfunction; Brain Neoplasms; Carcinoma, Bronchogenic; Carcinoma, Hepatocellular; Carcinoma, Small Cell; Cysts; Diagnosis, Differential; Fibroma; Hemangiosarcoma; Humans; Hyperparathyroidism; Hypoglycemia; Kidney Diseases; Kidney Neoplasms; Liver Neoplasms; Lung Neoplasms; Paraneoplastic Endocrine Syndromes; Pheochromocytoma; Polycythemia; Sarcoma; Thoracic Neoplasms; Vasopressins

Topics: Administration, Oral; Adolescent; Child; Child, Preschool; Chlorpropamide; Diabetes Insipidus; Diuresis; Female; Growth Hormone; Humans; Hypoglycemia; Lymphatic Diseases; Male; Sex Factors; Vasopressins

Topics: Chlorpropamide; Diabetes Insipidus; Drug Synergism; Humans; Hypoglycemia; Osmolar Concentration; Vasopressins

Topics: Chlorpropamide; Diabetes Insipidus; Humans; Hypoglycemia; Vasopressins

Topics: Adrenocorticotropic Hormone; Adult; Aged; Arthroplasty; Female; Humans; Hydrocortisone; Hypoglycemia; Insulin; Male; Middle Aged; Pituitary-Adrenal System; Stress, Physiological; Surgical Procedures, Operative; Vasopressins

Topics: Adolescent; Adrenocorticotropic Hormone; Anesthesia, General; Birth Injuries; Central Nervous System; Child; Child, Preschool; Dwarfism, Pituitary; Female; Humans; Hydrocortisone; Hypoglycemia; Insulin; Male; Metyrapone; Pituitary-Adrenal Function Tests; Vasopressins

Topics: Animals; Depression, Chemical; Feedback; Female; Growth Hormone; Haplorhini; Hypoglycemia; Insulin; Pituitary Gland; Vasopressins

Topics: Animals; Depression, Chemical; Dexamethasone; Female; Growth Hormone; Haplorhini; Hydrocortisone; Hypoglycemia; Insulin; Vasopressins

Topics: Adolescent; Adult; Chlorpropamide; Diabetes Insipidus; Diazoxide; Drinking Behavior; Female; Humans; Hypoglycemia; Kidney Tubules; Long-Term Care; Male; Middle Aged; Nephritis, Interstitial; Polyuria; Psychophysiologic Disorders; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adolescent; Aldosterone; Blood Glucose; Child; Child, Preschool; Chlorpropamide; Creatinine; Diabetes Insipidus; Female; Glomerular Filtration Rate; Glucose Tolerance Test; Humans; Hypoglycemia; Insulin; Male; Osmolar Concentration; Potassium; Sodium; Vasopressins

Topics: Adolescent; Child; Child, Preschool; Chlorpropamide; Diabetes Insipidus; Drug Synergism; Female; Humans; Hypoglycemia; Male; Vasopressins

Topics: Adolescent; Diabetes Insipidus; Growth; Growth Disorders; Growth Hormone; Humans; Hypoglycemia; Insulin; Insulin Antibodies; Male; Pituitary Function Tests; Skin Manifestations; Thyroxine; Vasopressins

Topics: Arthritis, Rheumatoid; Female; Glucocorticoids; Humans; Hypoglycemia; Injections, Intramuscular; Injections, Intravenous; Insulin; Lysine; Male; Pituitary-Adrenal Function Tests; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adolescent; Adult; Blood Glucose; Brain Neoplasms; Female; Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Insulin; Male; Meningioma; Metyrapone; Pituitary Function Tests; Sex Factors; Sodium Chloride; Vasopressins

Topics: Adult; Chlorpropamide; Depression, Chemical; Diabetes Insipidus; Diuresis; Humans; Hypoglycemia; Male; Stimulation, Chemical; Tannins; Vaccination; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adenoma; Adolescent; Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Adult; Circadian Rhythm; Cushing Syndrome; Dexamethasone; Diagnosis, Differential; Female; Humans; Hydrocortisone; Hyperplasia; Hypoglycemia; Hypothalamo-Hypophyseal System; Male; Metyrapone; Middle Aged; Pituitary-Adrenal Function Tests; Pituitary-Adrenal System; Secretory Rate; Vasopressins

Topics: Adrenocorticotropic Hormone; Blood Glucose; Endocrine Glands; Female; Humans; Hydrocortisone; Hypoglycemia; Insulin; Lysine; Male; Multiple Sclerosis; Nervous System Diseases; Pituitary-Adrenal Function Tests; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adolescent; Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Blood Glucose; Child; Child, Preschool; Female; Growth Disorders; Growth Hormone; Humans; Hypoglycemia; Infant; Insulin; Male; Metyrapone; Obesity; Pituitary Diseases; Pituitary-Adrenal Function Tests; Psychosexual Development; Puberty; Puberty, Precocious; Urine; Vasopressins; Virilism

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Blood Glucose; Dexamethasone; Diabetes Mellitus; Electroconvulsive Therapy; Ethylamines; General Surgery; Growth Hormone; Humans; Hypoglycemia; Insulin; Metabolism; Pituitary Gland; Pyrazoles; Radioimmunoassay; Stress, Physiological; Vasopressins

Topics: Animals; Dogs; Glucose; Hyperglycemia; Hypoglycemia; Insulin; Lipid Metabolism; Metabolism; Oxytocin; Peptides; Rabbits; Vasopressins

Topics: Arginine; Child; Deficiency Diseases; Endocrine System Diseases; Fasting; Growth; Growth Disorders; Growth Hormone; Humans; Hypoglycemia; Hypothyroidism; Insulin; Radioimmunoassay; Stimulation, Chemical; Turner Syndrome; Vasopressins

Topics: Adenoma; Adrenocorticotropic Hormone; Adult; Aged; Cerebral Ventriculography; Female; Humans; Hydrocortisone; Hypoglycemia; Insulin; Male; Metyrapone; Middle Aged; Pituitary Neoplasms; Pituitary-Adrenal Function Tests; Pyrogens; Vasopressins

Topics: Adolescent; Adrenocorticotropic Hormone; Child; Child, Preschool; Dexamethasone; Humans; Hydrocortisone; Hypoglycemia; Hypothalamo-Hypophyseal System; Insulin; Pituitary-Adrenal Function Tests; Pituitary-Adrenal System; Prednisone; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Catheterization; Charcoal; Dexamethasone; Female; Hypoglycemia; Insulin; Jugular Veins; Lysine; Metyrapone; Radioimmunoassay; Stress, Physiological; Swine; Vasopressins

Topics: Acromegaly; Animals; Epinephrine; Glucose Tolerance Test; Growth Hormone; Haplorhini; Humans; Hypoglycemia; Hypothalamo-Hypophyseal System; Models, Biological; Pituitary Gland; Prochlorperazine; Temperature; Umbilical Cord; Vasopressins

Topics: Animals; Arousal; Blood Glucose; Chlorpromazine; Fatty Acids, Nonesterified; Growth Hormone; Haplorhini; Hemorrhage; Histamine; Hypoglycemia; Morphine; Pentobarbital; Vasopressins

Topics: Adrenalectomy; Animals; Arginine; Cats; Dogs; Glucagon; Hepatectomy; Hypoglycemia; Hypophysectomy; Insulin; Lysine; Pancreatectomy; Perfusion; Rabbits; Vasopressins

Topics: Acetohexamide; Chlorpropamide; Depression, Chemical; Diabetes Insipidus; Diuresis; Humans; Hydrochlorothiazide; Hypoglycemia; Osmolar Concentration; Phenformin; Polythiazide; Sodium Chloride; Urine; Vasopressins

Topics: Arthritis, Rheumatoid; Humans; Hypoglycemia; Hypothalamo-Hypophyseal System; Insulin; Lysine; Middle Aged; Pituitary-Adrenal System; Steroids; Triamcinolone; Vasopressins

Topics: Animals; Arginine; Dogs; Hypoglycemia; Pancreatectomy; Perfusion; Vasopressins

The insulin test carried out with adequate safeguards under standardized conditions yields valuable information regarding hypothalamic and pituitary function when plasma levels of sugar, cortisol, and growth hormone are determined. The use of a test based on the plasma cortisol response to the infusion of lysine-vasopressin, a polypeptide with a corticotrophin-releasing action, is also of value as a test of pituitary function. Used in conjunction with the insulin test it enables pituitary disorders to be differentiated from those involving the hypothalamus.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Blood; Child; Diagnosis, Differential; Endocrine System Diseases; Female; Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Hypothalamo-Hypophyseal System; Hypothalamus; Insulin; Lysine; Male; Pituitary Diseases; Pituitary Function Tests; Stress, Physiological; Urine; Vasopressins

Topics: Adolescent; Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Adult; Child; Diabetes Insipidus; Female; Humans; Hyperinsulinism; Hypoglycemia; Hypothalamus; Male; Vasopressins

Topics: Animals; Blood Glucose; Dogs; Fatty Acids; Female; Glucose; Hypoglycemia; Male; Vasopressins

Topics: 5-Hydroxytryptophan; Carcinoid Tumor; Carcinoma, Hepatocellular; Carotid Body Tumor; Catecholamines; Cushing Syndrome; Endocrine System Diseases; Female; Fibrosarcoma; Humans; Hyperthyroidism; Hypoglycemia; Hyponatremia; Liver Neoplasms; Lung Neoplasms; Male; Neoplasms; Polycythemia Vera; Puberty, Precocious; Vasopressins

Topics: Carcinoid Tumor; Cushing Syndrome; Humans; Hyperthyroidism; Hypoglycemia; Neoplasms; Pheochromocytoma; Polycythemia; Puberty; Puberty, Precocious; Sexual Maturation; Vasopressins