pituitrin and Diabetes-Mellitus

The diabetic kidney disease (DKD) is the major cause of the chronic kidney disease (CKD). Enhanced plasma vasopressin (VP) levels have been associated with the pathophysiology of DKD and CKD. Stimulation of VP release in DKD is caused by glucose-dependent reset of the osmostat leading to secondary pathophysiologic effects mediated by distinct VP receptor types. VP is a stress hormone exhibiting the antidiuretic action in the kidney along with broad adaptive effects in other organs. Excessive activation of the vasopressin type 2 (V2) receptor in the kidney leads to glomerular hyperfiltration and nephron loss, whereas stimulation of vasopressin V1a or V1b receptors in the liver, pancreas, and adrenal glands promotes catabolic metabolism for energy mobilization, enhancing glucose production and aggravating DKD. Increasing availability of selective VP receptor antagonists opens new therapeutic windows separating the renal and extra-renal VP effects for the concrete applications. Improved understanding of these paradigms is mandatory for further drug design and translational implementation. The present concise review focuses on metabolic effects of VP affecting DKD pathophysiology.

Topics: Diabetes Mellitus; Diabetic Nephropathies; Glucose; Humans; Receptors, Vasopressin; Renal Insufficiency, Chronic; Vasopressins

Orthostatic hypertension-a condition characterized by a hyperactive pressor response to orthostatic stress-is an emerging risk factor for cardiovascular disease and is associated with hypertensive target-organ damage (resulting in silent cerebrovascular disease, left ventricular hypertrophy, carotid atherosclerosis and/or chronic kidney disease) and cardiovascular events (such as coronary artery disease and lacunar stroke). The condition is also considered to be a form of prehypertension as it precedes hypertension in young, normotensive adults. Orthostatic blood pressure changes can be assessed using orthostatic stress tests, including clinic active standing tests, home blood pressure monitoring and the head-up tilting test. Devices for home and for ambulatory blood pressure monitoring that are equipped with position sensors and do not induce a white-coat effect have increased the sensitivity and specificity of diagnosis of out-of-clinic orthostatic hypertension. Potential major mechanisms of orthostatic hypertension are sympathetic hyperactivity (as a result of hypersensitivity of the cardiopulmonary and arterial baroreceptor reflex) and α-adrenergic hyperactivation. Orthostatic hypertension is also associated with morning blood pressure surge and extreme nocturnal blood pressure dipping, both of which increase the pulsatile haemodynamic stress of central arterial pressure and blood flow in patients with systemic haemodynamic atherothrombotic syndrome.

Topics: Age Factors; Arteriosclerosis; Blood Pressure Monitoring, Ambulatory; Blood Volume; Brain Infarction; Cardiovascular Diseases; Diabetes Mellitus; Hemodynamics; Humans; Hypertriglyceridemia; Hypotension, Orthostatic; Posture; Prehypertension; Receptors, Adrenergic, alpha; Renal Insufficiency, Chronic; Risk Factors; Sympathetic Nervous System; Thrombosis; Tilt-Table Test; Vasopressins; Ventricular Remodeling

Topics: Animals; Atrial Natriuretic Factor; Biological Transport; Bradykinin; Calcium; Calcium Channels; Cyclooxygenase 2; Diabetes Mellitus; Diabetic Nephropathies; Glomerular Filtration Rate; Humans; Kidney Tubules; Membrane Proteins; Muscle Tonus; Muscle, Smooth, Vascular; Nitric Oxide; Prostaglandin-Endoperoxide Synthases; Renal Circulation; Renin-Angiotensin System; Sodium; Vasopressins

Urea is transported across the kidney inner medullary collecting duct by urea-transporter proteins. Two urea-transporter genes have been cloned from humans and rodents: the UT-A (Slc14A2) gene encodes five protein and eight cDNA isoforms; the UT-B (Slc14A1) gene encodes a single isoform. In the past year, significant progress has been made in understanding the regulation of urea-transporter protein abundance in kidney, studies of genetically engineered mice that lack a urea transporter, identification of urea transporters outside of the kidney, cloning of urea transporters in nonmammalian species, and active urea transport in microorganisms.. UT-A1 protein abundance is increased by 12 days of vasopressin, but not by 5 days. Analysis of the UT-A1 promoter suggests that vasopressin increases UT-A1 indirectly following a direct effect to increase the transcription of other genes, such as the Na(+)-K(+)-2Cl- cotransporter NKCC2/BSC1 and the aquaporin (AQP) 2 water channel, that begin to increase inner medullary osmolality. UT-A1 protein abundance is also increased by adrenalectomy, and is decreased by glucocorticoids or mineralocorticoids. However, each hormone works through its own receptor. Knockout mice that lack UT-A1 and UT-A3, or lack UT-B, have a urine-concentrating defect and a decrease in inner medullary interstitial urea content.. Urea transporters play a critical role in the urine-concentrating mechanism. Their abundance is regulated by vasopressin, glucocorticoids, and mineralocorticoids. These regulatory mechanisms may be important in disease states such as diabetes because changes in urea-transporter abundance in diabetic rats require glucocorticoids and vasopressin.

Topics: Animals; Diabetes Mellitus; Humans; Kidney; Kidney Tubules, Collecting; Membrane Transport Proteins; Urea Transporters; Vasopressins

Physiologic data provided evidence for specific urea transporter proteins in red blood cells and kidney inner medulla. During the past decade, molecular approaches resulted in the cloning of several urea transporter cDNA isoforms derived from two gene families: UT-A and UT-B. Polyclonal antibodies were generated to the cloned urea transporter proteins, and their use in integrative animal studies resulted in several novel findings, including: (1) UT-B is the Kidd blood group antigen; (2) UT-B is also expressed in many non-renal tissues and endothelial cells; (3) vasopressin increases UT-A1 phosphorylation in rat inner medullary collecting duct; (4) the surprising finding that UT-A1 protein abundance and urea transport are increased in the inner medulla during conditions in which urine concentrating ability is reduced; and (5) UT-A protein abundance is increased in uremia in both liver and heart. This review will summarize the knowledge gained from studying molecular mechanisms of urea transport and from integrative studies into urea transporter protein regulation.

Topics: Angiotensins; Animals; Biological Transport, Active; Cell Membrane Permeability; Diabetes Mellitus; Homeostasis; Humans; Kidney; Kidney Concentrating Ability; Kidney Medulla; Membrane Transport Proteins; Mice; Rats; Renal Insufficiency; Urea; Urea Transporters; Uremia; Urine; Vasopressins

Diabetes mellitus increases the risk for hypertension and associated cardiovascular diseases, including coronary, cerebrovascular, renal and peripheral vascular disease. The risk for developing cardiovascular disease is increased when both diabetes and hypertension co-exist; in fact, over 11 million Americans have both diabetes and hypertension. These numbers will continue to climb, internationally, since the leading associated risk for diabetes development, obesity, has reached epidemic proportions, globally. Moreover, the frequent association of diabetes with dyslipidemia, as well as coagulation, endothelial, and metabolic abnormalities also aggravates the underlying vascular disease process in patients who possess these comorbid conditions. The renin-angiotensin-aldosterone system (RAS) and arginine vasopressin (AVP) are overactivated in both hypertension and diabetes. Drugs that inhibit this system, such as ACE inhibitors and more recently angiotensin receptor antagonists (ARBs), have proven beneficial effects on the micro- and macrovascular complications of diabetes, especially the kidney. The BRILLIANT study showed that lisinopril reduces microalbuminuria better than CCB therapy. Numerous other long-term studies confirm this association with ACE inhibitors including the HOPE trial. Furthermore, the European Controlled trial of Lisinopril in Insulin-dependent Diabetes (EUCLID) study, showed that lisinopril slowed the progression of renal disease, even in individuals with mild albuminuria. In fact, there are now five appropriately powered randomized placebo-controlled trials to show that both ACE inhibitors and ARBs slow progression of diabetic nephropathy in people with type 2 diabetes. These effects were shown to be better than conventional blood pressure lowering therapy, including dihydropyridine CCBs. In patients with microalbuminuria, ACE inhibitors and ARBs reduce the progression of microalbuminuria to proteinuria and provide a risk reduction of between 38 and 60% for progression to proteinuria. This is important since microalbuminuria is known to be associated with increased vascular permeability and decreased responsiveness to vasodilatory stimuli. Recently, increased AVP levels have been lined to microalbuminuria and hyperfiltration in diabetes. The microvascular and macrovascular benefits of ACE inhibition, ARBs and possible role of AVP antagonists in diabetic patients will be discussed, as will be recommendations for its clinical use.

Topics: Aldosterone; Angiotensin-Converting Enzyme Inhibitors; Aquaporins; Cardiovascular System; Diabetes Mellitus; Diabetic Angiopathies; Diabetic Nephropathies; Diuretics; Humans; Risk Factors; Vasopressins

Thirst and drinking are essential components of normal osmoregulation in healthy man. Abnormalities of thirst appreciation, in particular hypodipsia, have profound implications for water homeostasis. The combination of cranial diabetes insipidus and hypodipsia can have particularly serious consequences, with the potential for life-threatening hyponatraemia. Although the tools for measuring thirst are subjective and lack true specificity, their use in clinical research has contributed greatly to our understanding of the physiology of thirst appreciation and the abnormal control of thirst in osmoregulatory disorders. The precise neural control of thirst appreciation remains unknown, and perhaps as a result of this, satisfactory therapies for the treatment of disorders of thirst have not yet been developed; behavioural modification and retraining of drinking habits remain the rather limited cornerstones of management.

Topics: Adult; Aged; Aging; Brain Neoplasms; Diabetes Insipidus; Diabetes Mellitus; Drinking; Humans; Inappropriate ADH Syndrome; Middle Aged; Schizophrenia; Thirst; Vasopressins; Water-Electrolyte Balance

Of the many information obtainable from the urine of diabetic patients, urinary C-peptide (CPR), albumin and anti-diuretic hormone (ADH) were representatively described using my clinical and experimental data. C-peptide excretion in 24h collection of urine is a good estimate of insulin secretion from the pancreas and thus low in IDDM patients and even in NIDDM patients at a later stage, but high in pathological conditions including Graves' disease, obesity, liver cirrhosis and Cushing's syndrome. Urinary albumin excretion in small amounts (microalbuminuria) is usually observed in diabetic patients who have been under a poor control state of diabetic hyperglycemia for over 5 years and provides a good tool for monitoring early diabetic nephropathy. The grade of microalbuminuria (30-300 mg/day) is positively correlated with the HbA1 level in diabetic patients, showing that microalbuminuria is reversible along with an improvement of diabetic control at least in an early phase of diabetic nephropathy. As the albumin level measured in a spot urine sample correlates well with the value in the 24h collection of urine, the albumin measurement is conveniently feasible with a spot urine sample at every patient's visit. The amount of ADH excreted in urine is 7-10% of that secreted from the posterior pituitary. The excretion of ADH in a day was in the urine of diabetic patients positively correlated with HbA1, urinary osmolarity and concentration of sodium in urine, although the pathological meaning of the observed ADH hypersecretion in the development of diabetic complications is currently unknown.

Topics: Albuminuria; C-Peptide; Diabetes Complications; Diabetes Mellitus; Humans; Vasopressins

Topics: Adrenocorticotropic Hormone; Diabetes Mellitus; Dose-Response Relationship, Drug; Drug Resistance; Endocrine System Diseases; Gonadotropins; Hormones; Humans; Insulin Resistance; Neuromuscular Diseases; Obesity; Parathyroid Hormone; Receptor, Insulin; Receptors, Cell Surface; Syndrome; Thyrotropin; Vasopressins

Topics: Adrenal Cortex Hormones; Adrenal Glands; Calcitonin; Carbohydrate Metabolism; Diabetes Mellitus; Endocrine Glands; Ethanol; Female; Humans; Hypocalcemia; Lipid Metabolism; Male; Metabolism; Somatostatin; Testis; Vasopressins

Topics: Angiotensins; Catecholamines; Diabetes Mellitus; Hemorrhage; Hormones; Humans; Liver; Obesity; Phosphorylases; Shock; Vasopressins

Topics: Animals; Anura; Chlorpropamide; Diabetes Insipidus; Diabetes Mellitus; Dogs; Humans; Prostaglandins E; Rabbits; Rats; Urinary Bladder; Vasopressins

The authors present a brief review of the problem of diabetes insipidus in neurosurgical patients, with particular emphasis on the differential diagnosis of postoperative and posttraumatic polyuria and the management of diabetes insipidus in these periods. A listing of drugs currently used in its treatment is given.

Topics: Administration, Intranasal; Benzothiadiazines; Brain Injuries; Carbamazepine; Chlorpropamide; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Mellitus; Diagnosis, Differential; Diuretics; Humans; Hypothalamo-Hypophyseal System; Lypressin; Methods; Polyuria; Postoperative Complications; Sodium Chloride Symporter Inhibitors; Vasopressins; Water-Electrolyte Balance

Topics: Acetaminophen; Amitriptyline; Animals; Anura; Body Fluids; Carbamazepine; Chlorpropamide; Clofibrate; Cyclophosphamide; Diabetes Insipidus; Diabetes Mellitus; Diazoxide; Drug-Related Side Effects and Adverse Reactions; Humans; Hypoglycemic Agents; Hyponatremia; Kidney; Rats; Sodium; Sulfonylurea Compounds; Tolbutamide; Urinary Bladder; Vasopressins; Vincristine; Water Intoxication; Water-Electrolyte Balance

Glyburide is an improved drug for the management of non-insulin-dependent diabetes mellitus (NIDDM). It is at least as effective as the first-generation oral hypoglycemics and is effective in doses that are considerably less than those needed with first-generation sulfonyl-ureas. While its mode of action is similar to that of other agents, glyburide has the unique feature of prolonged activity despite a short half-life and short duration in the body. Side effects are minimal, and toxic reactions have not been reported. While hypoglycemic episodes can occur, as with any blood glucose-lowering agent, they can be prevented by being alert to patients who may be more sensitive to oral agents. Unlike older sulfonylureas, about 50% of glyburide is excreted through the feces. In 14 years of worldwide experience, glyburide has rarely shown disulfiram-like effects and has not shown antidiuretic effects. While glyburide produces an insulin release response to glucose that parallels a normal physiological response, it appears to also decrease resistance to insulin and sensitize the receptors while utilizing the patient's available endogenous insulin. There are two major metabolites, but they are inert and are rapidly excreted, having no hypoglycemic effect. Considering the safety of glyburide and the large worldwide population that uses this agent, it is expected that this new second-generation hypoglycemic agent will greatly increase the therapeutic spectrum for NIDDM. Not only is it possible for more patients with diabetes to be treated, but many already being treated orally can achieve better regulation with this effective new oral agent.

Topics: Animals; Biological Availability; Blood Coagulation; Cardiovascular System; Clinical Trials as Topic; Diabetes Mellitus; Glyburide; Humans; Kidney; Liver; Platelet Aggregation; Protein Binding; Vasopressins

Topics: Clinical Trials as Topic; Diabetes Insipidus; Diabetes Mellitus; Diuresis; Diuretics; Glomerular Filtration Rate; Glyburide; Humans; Lysine; Vasopressins

Topics: Adrenal Glands; Adrenalectomy; Adult; Aged; Blood Glucose; Clinical Trials as Topic; Cyclic AMP; Diabetes Mellitus; Female; Glucosyltransferases; Growth Hormone; Humans; Insulin; Male; Middle Aged; Vasopressins

Familial pituitary diabetes insipidus has been described only in an autosomal dominant or recessive mode of inheritance.. This work aims to determine the cause of a novel form of familial diabetes insipidus (DI) that is controlled by desmopressin therapy but segregates in an X-linked recessive manner.. Thirteen members from 3 generations of the kindred with familial DI were studied. Water intake, urine volume, urine osmolality, plasma osmolality, and plasma vasopressin were measured under basal conditions, during fluid deprivation, 3% saline infusion, and water loading. Magnetic resonance images of the posterior pituitary also were obtained. In affected males, the effects of desmopressin therapy and linkage of the DI to markers for chromosome Xq28 were determined. In addition, the genes encoding vasopressin, aquaporin-2, the AVPR2 receptor, and its flanking regions were sequenced.. This study showed that 4 males from 3 generations of the kindred have DI that is due to a deficiency of vasopressin, is corrected by standard doses of desmopressin, and segregates with markers for the AVPR2 gene in Xq28. However, no mutations were found in AVPR2 or its highly conserved flanking regions. Exome sequencing confirmed these findings and also revealed no deleterious variants in the provasopressin and aquaporin-2 genes. The 4 obligate female carriers osmo-regulated vasopressin in the low normal range.. X-linked recessive transmission of DI can be due to a defect in either the secretion or the action of vasopressin. Other criteria are necessary to differentiate and manage the 2 disorders correctly.

Topics: Aquaporin 2; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Mellitus; Female; Humans; Male; Receptors, Vasopressin; Vasopressins

We studied the growth dynamics of Walker 256 carcinosarcoma in recombinant progeny of dihybrid crosses of Brattleboro and WAG rats. A mutation in the vasopressin gene determining hypothalamic diabetes insipidus was detected in Brattleboro rats. WAG rats are carriers of normal vasopressin gene. Another interlinear difference was linked to tyrosinase gene controlling melanin synthesis. WAG rats express mutant allele determining albino phenotype. Brattleboro rats had normal working tyrosinase gene. F2 segregation yielded phenotypic classes with two patterns of tumor growth: linear growth or regression. Tumors regression was not linked to tyrosinase activity and was observed only in rats with diabetes insipidus. Analysis of mutants in next generations F3 and F4 confirmed this regularity in the Walker 256 carcinosarcoma growth pattern.

Topics: Animals; Carcinoma 256, Walker; Carcinosarcoma; Diabetes Insipidus; Diabetes Mellitus; Melanins; Monophenol Monooxygenase; Rats; Rats, Brattleboro; Vasopressins

Water homeostasis is tightly regulated by the kidneys via the process of urine concentration. During reduced water intake, the antidiuretic hormone arginine vasopressin (AVP) binds to the vasopressin receptor type II (V2R) in the kidney to enhance countercurrent multiplication and medullary osmolality, and increase water reabsorption via aquaporin-2 (AQP2) water channels. The importance of this AVP, V2R, and AQP2 axis is highlighted by low urine osmolality and polyuria in people with various water balance disorders, including nephrogenic diabetes insipidus (NDI). ELF5 and nuclear factor of activated T cells 5 (NFAT5) are two transcription factors proposed to regulate Aqp2 expression, but their role is poorly defined. Here we generated two novel mouse lines with principal cell (PC)-specific deletion of ELF5 or NFAT5 and phenotyped them in respect to renal water handling. ELF5-deficient mice (ELF5

Topics: Animals; Aquaporin 2; Arginine Vasopressin; Deamino Arginine Vasopressin; Diabetes Insipidus, Nephrogenic; Diabetes Mellitus; Factor V; Kidney Tubules, Collecting; Mice; Receptors, Vasopressin; T-Lymphocytes; Transcription Factors; Vasopressins; Water

A 49-year-old man developed severe hyponatremia associated with transient headache and was diagnosed with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Fluid restriction and sodium supplementation corrected the hyponatremia. However, several days later, the patient exhibited hypernatremia with thirst and polyuria. A detailed examination indicated central diabetes insipidus (CDI) with an intrasellar cystic lesion indicative of Rathke's cleft cyst (RCC). A case of RCC exhibiting headache, hyponatremia, and subsequent hypernatremia has been reported. Our case shows that CDI may appear after SIADH in patients with RCC, especially in those with serum sodium levels that unexpectedly increase rapidly beyond the reference range.

Topics: Central Nervous System Cysts; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

Familial neurohypophyseal diabetes insipidus (FNDI) is a rare disorder characterized by childhood-onset progressive polyuria and polydipsia due to mutations in the arginine vasopressin (AVP) gene. The aim of the study was to describe the clinical and molecular characteristics of families with neurohypophyseal diabetes insipidus.. Five Portuguese families with autosomal dominant FNDI underwent sequencing of the AVP gene and the identified mutations were functionally characterized by in vitro studies.. Three novel and two recurrent heterozygous mutations were identified in the AVP gene. These consisted of one initiation codon mutation in the signal peptide coding region (c.2T > C, p.Met1?), three missense mutations in the neurophysin II (NPII) coding region (c.154T > C, p.Cys52Arg; c.289C > G, p.Arg97Gly; and c.293G > C, p.Cys98Ser), and one nonsense mutation in the NPII coding region (c.343G > T, p.Glu115Ter). In vitro transfection of neuronal cells with expression vectors containing each mutation showed that the mutations resulted in intracellular retention of the vasopressin prohormone. Patients showed progressive symptoms of polyuria and polydipsia, but with wide variability in severity and age at onset. No clear genotype-phenotype correlation was observed.. The intracellular accumulation of mutant vasopressin precursors supports the role of cellular toxicity of the mutant proteins in the etiology of the disorder and explains the progressive onset of the disorder. These findings further expand the AVP mutational spectrum in FNDI and contribute to the understanding of the molecular pathogenic mechanisms involved in FNDI.

Topics: Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Mutation; Neurophysins; Pedigree; Polydipsia; Polyuria; Vasopressins

Topics: Diabetes Insipidus; Diabetes Mellitus; Humans; Vasopressins

Topics: Diabetes Insipidus; Diabetes Mellitus; Humans; Vasopressins

There are two forms of diabetes insipidus, central (neurohypophyseal), and nephrogenic, caused by pathogenic variants in the AVP gene and the AVPR2 or AQP2 genes, respectively. We report on a four-generation family, seven individuals had central diabetes insipidus (CDI) and the female index patient seen from age 16 to 26 years had (mild) nephrogenic diabetes insipidus. In her father with CDI, a known pathogenic heterozygous AVP variant c.232_234del p.(Glu78del) was identified, confirming the diagnosis of CDI in him and the other affected family members. In the proband, molecular analysis disclosed a novel heterozygous AVPR2 gene variant, c.962A > T p.(Asn321Ile) and an extremely skewed X-inactivation, confirming X-linked nephrogenic diabetes insipidus (XL-NDI). Whole exome sequencing showed no further causative mutation. This is the first report on the co-existence of CDI and NDI in one family. Our review of symptomatic female AVPR2 heterozygotes includes 23 families with at least one affected female (including this study). There were 21 different causative mutations. Mutation types in females did not differ from those in males. Both severe XL-NDI and mild forms were reported in females. All six females with severe XL-NDI had complete loss-of-function (null) mutations. The remaining 17 female probands had milder XL-NDI caused by 14 missense variants and three null variants of the AVPR2 gene. X-inactivation was studied in nine of these females; all showed extreme or slight skewing. The review underlines that XL-NDI in female AVPR2 heterozygotes is always accompanied by skewed X-inactivation, emphasizing a need for X-inactivation studies in these females.

Topics: Adolescent; Adult; Aquaporin 2; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Exome Sequencing; Female; Genes, X-Linked; Humans; Male; Mutation, Missense; Neurophysins; Pedigree; Protein Precursors; Receptors, Vasopressin; Vasopressins; X Chromosome Inactivation; Young Adult

Cardioplegic arrest (CP) and cardiopulmonary bypass (CPB) are associated with vasomotor dysfunction of coronary arterioles in patients with diabetes (DM) undergoing cardiac surgery. We hypothesized that DM may up-regulate vasopressin receptor expression and alter the contractile response of coronary arterioles to vasopressin in the setting of CP/CPB.. Right atrial tissue samples of patients with DM and without (ND) (n = 8 in each group) undergoing cardiac surgery were harvested before and after CP/CPB. The isolated coronary arterioles (80-150 μm) dissected from the harvested right atrial tissue samples were cannulated and pressurized (40 mm Hg) in a no-flow state. The changes in diameter were measured with video microscopy. The protein expression/localization of vasopressin 1A receptors (V1A) and vasopressin 1B receptors (V1B) in the atrial tissue were measured by immune-blotting and immunohistochemistry.. CP/CPB and DM are both associated with up-regulation in V1 receptor expression/localization in human myocardium. Vasopressin may induce coronary arteriolar constriction via V1A. This alteration may lead to increased coronary arteriolar spasm in patients with DM undergoing CP/CPB and cardiac surgery.

Topics: Aged; Arterioles; Cardiopulmonary Bypass; Case-Control Studies; Coronary Artery Bypass; Coronary Vasospasm; Coronary Vessels; Diabetes Mellitus; Female; Heart Arrest, Induced; Humans; Male; Middle Aged; Receptors, Vasopressin; Signal Transduction; Up-Regulation; Vasoconstriction; Vasoconstrictor Agents; Vasopressins

Topics: Constriction; Diabetes Mellitus; Heart Atria; Humans; Vasopressins

In the last decade, cross-sectional and multiple cohort studies have associated total fluid intake or water intake with the risk for chronic kidney disease (CKD) and even the risk of developing hyperglycemia. Urine biomarkers have also been linked to the risk of CKD and lithiasis, and these biomarkers respond quickly to variations in fluid intake. High circulating copeptin levels, a surrogate marker of arginine vasopressin, have been associated with metabolic syndrome, renal dysfunction and increased risk for diabetes mellitus, cardiovascular disease and death. The aim of this paper was to explore how the various findings on water intake, hydration and health are interconnected, to highlight current gaps in our understanding and to propose a model that links water intake, homeostatic mechanisms to maintain water balance and health outcomes. Since plasma copeptin and vasopressin have been demonstrated to be sensitive to changes in water intake, inversely associated with 24-hour urine volume, and associated with urine biomarkers and fluid intake, vasopressin is proposed as the central player in this theoretical physiological model.

Topics: Arginine Vasopressin; Biomarkers; Cardiovascular Diseases; Diabetes Mellitus; Drinking; Glycopeptides; Health Status; Humans; Hyperglycemia; Metabolic Syndrome; Models, Biological; Renal Insufficiency, Chronic; Risk Factors; Vasopressins; Water-Electrolyte Balance

It has been well known that several neuropeptides may affect human behavior, and that some endocrinopathies are associated with impaired higher function of the brain. There have been increasing evidences that vasopressin has both peripheral and central effects, the latter of which is involved in memory. In experimental animals, male mice with a null mutation in the V1a receptor (V1aR) exhibit a profound impairment in social recognition and changes in anxiety-like behavior. An AVP fragment analog has been reported to facilitate memory retention and recall in mice through protein kinase C-independent pathways. In human, a few recent reports have suggested that a familial central diabetes insipidus, caused by a heterozygous mutation in the gene for vasopressin prohormone, have minor disturbances in central nervous system. Taken together, it is hypothesized that the subject with central diabetes insipidus may frequently present with an impaired cognitive ability. It is justified to examine the cognitive function, when we make a diagnosis of central diabetes insipidus and to perform a clinical study to investigate whether central diabetes insipidus may be associated with impairment of higher brain functions.

Topics: Animals; Brain; Cognition; Diabetes Mellitus; Disease Models, Animal; Humans; Male; Mice; Neuropeptides; Vasopressins

Vasopressin, an antidiuretic hormone, is elevated in diabetes mellitus (DM). The aim of this study was to evaluate whether the V(2) receptor-mediated actions of vasopressin contribute to the albuminuria of diabetes.. Fourteen adult male Wistar rats with streptozotocin-induced DM were treated over 9 weeks with a selective, non-peptide, orally active V(2) receptor antagonist (SR 121463) and were compared to 14 untreated diabetic rats (control). The dose of antagonist was adapted in order to maintain urine osmolality close to plasma osmolality, but not to induce the formation of hypoosmotic urine. Every second week, urine was collected in metabolic cages for two 24 h periods.. Urinary albumin excretion (UAE) rose regularly and significantly with time in the untreated control group, whereas it did not rise in treated rats. Interestingly, a variable pattern of UAE increase over time was observed in different rats of the control group. Some rats exhibited pronounced progression of albuminuria with time, while others showed no or only a very modest rise. An a posteriori partition of the control group into 'progressors' and 'non-progressors' revealed that progressors had more intense urinary concentrating activity, higher creatinine clearance and larger relative glomerular mesangial area than the other subgroup.. This study shows that V(2) receptor-mediated actions of vasopressin play a critical role in the albuminuria of diabetes. It also reveals that individual rats, like humans, seem to exhibit an unequal susceptibility to diabetic nephropathy, or at least to albuminuria, a factor considered to be one of its early manifestations.

Topics: Albuminuria; Animals; Antidiuretic Hormone Receptor Antagonists; Diabetes Complications; Diabetes Mellitus; Diabetes Mellitus, Experimental; Kidney; Male; Morpholines; Rats; Rats, Wistar; Receptors, Vasopressin; Spiro Compounds; Streptozocin; Vasopressins

Although secondary end-organ damage in diabetes has generally been thought to result from long-term passive shunting of excess glucose through alternative metabolic pathways, recent studies have elucidated a second mechanism of pathogenesis that involves active changes in gene expression in neurons of the CNS. These changes in gene expression result in molecular and functional changes that can become maladaptive over time. In this review, we examine two neuronal populations in the brain that have been studied in human beings and animal models of diabetes. First, we discuss overactivation of magnocellular neurosecretory cells within the hypothalamus and how it relates to the development of diabetic nephropathy. And second, we describe how changes in hippocampal synaptic plasticity can lead to cognitive and behavioural deficits in chronic diabetes. Changes in neuronal gene expression in diabetes represent a new pathway for diabetic pathogenesis. This pathway may hold clues for the development of therapies that, via the targeting of neurons, can slow or prevent the development of diabetic end-organ damage.

Topics: Animals; Cognition Disorders; Diabetes Mellitus; Diabetic Nephropathies; Gene Expression; Hippocampus; Humans; Hyperglycemia; Hypothalamus; Neuronal Plasticity; Neurons; Vasopressins

We had the opportunity to closely observe a unique case of central diabetes insipidus (DI), in which dramatic changes in both radiological findings and hypophysial functions were seen. A 63-year-old female developed central DI, and magnetic resonance imaging (MRI) revealed a mild thickening of the pituitary stalk and lack of hyperintense signal associated with normal neurohypophysis on T1-weighted images. About three months later, the stalk was found to be remarkably expanded like neoplasm; however, anterior pituitary functions were almost normal on that occasion, except for the absence of GH response to an insulin tolerance test. About nine months after the onset of DI, secondary hypoadrenalism and hypothyroidism, which required replacement therapy, developed transiently, but recovered about one year later. Results of hypophysial endocrine tests during this period showed that the dysfunction was predominantly suprapituitary in nature. As time passed, the stalk lesion began to shrink spontaneously and another MRI, obtained five years after the onset of DI, disclosed normal findings for the infundibulo-hypophysial system, except for lack of the hyperintense signal of the neurohypophysis. The patient has since been healthy, except for the DI, which has been controlled by treatment with vasopressin. We report here a unique case of central DI associated with transient pituitary stalk enlargement.

Topics: Adrenocorticotropic Hormone; Corticotropin-Releasing Hormone; Diabetes Mellitus; Female; Gonadotropins, Pituitary; Human Growth Hormone; Humans; Hydrocortisone; Hydroxysteroids; Insulin; Magnetic Resonance Imaging; Middle Aged; Pituitary Gland; Pituitary Gland, Anterior; Prolactin; Radiography; Thyroxine; Triiodothyronine; Vasopressins

We studied osmoregulation of plasma vasopressin in 5 patients with newly diagnosed diabetes mellitus. All patients showed typical symptoms of uncontrolled diabetes mellitus such as marked hyperglycemia, polyuria, and polydipsia, but did not have advanced diabetic complications. Vasopressin release was studied using 5% hypertonic saline infusion test twice: before treatment when the patient was hyperglycemic, and after treatment 1 to 2 months later when the patient was euglycemic. Plasma vasopressin was measured by a sensitive and specific radioimmunoassay. The mean basal plasma vasopressin value in the patients was significantly higher in the hyperglycemic compared with the euglycemic state (3.75 +/- 0.70 vs 1.18 +/- 0.46 pmol/l, respectively; P < 0.05). The relationship of plasma vasopressin with serum sodium, but not plasma osmolality, during hyperglycemia showed an apparent hypersecretion of vasopressin. In both cases, the sensitivity of the vasopressin response to osmotic stimuli was significantly decreased. During euglycemia, the sensitivity of vasopressin secretion to either sodium or osmolality was almost normal, although a slight rise in the osmostat was observed compared with normal subjects. Together, we found that the positive correlation of vasopressin with sodium or osmolality is maintained but significantly altered in patients with untreated diabetes mellitus. Especially noteworthy is the lowered threshold and decreased sensitivity of osmotically-induced vasopressin secretion during hyperglycemia, which may be caused by multiple factors such as diabetes-associated hypovolemia, osmogenic effects of glucose and other osmoles, depletion of the pool of vasopressin available for release, and the metabolic derangement of osmoreceptor/magnocellular neurons.

Topics: Adult; Blood Glucose; Diabetes Mellitus; Female; Humans; Hyperglycemia; Hypertonic Solutions; Male; Middle Aged; Sodium; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Chlorpropamide (CPM) has been reported to produce impaired water excretion due to the enhancement of renal vasopressin (ADH) action and/or due to centrally enhanced ADH release, but it is still unknown whether CPM gives rise to ADH release with a subsequent hyponatremia in diabetes mellitus (DM), which, in turn, causes an impairment of the central nervous system. In 3 patients with DM, who developed hyponatremia during the treatment with CPM, an acute water load (WL) was carried out in the presence and absence of the drug, and plasma ADH was determined with plasma and urine osmolalities. Moreover, in 2 cases, MRI scans of the brain were taken. In all the patients, acute WL tests failed to suppress completely ADH release in response to changes in plasma osmolality in the presence of CPM, which, in turn, resulted in the impaired water excretion. In the absence of CPM, an acute WL normally suppressed plasma ADH leading to the diuresis. MRI scans illustrated the presence of central pontine myelinolysis. It is likely that CPM might stimulate ADH release in DM with a subsequent hyponatremia and brain damages.

Topics: Aged; Chlorpropamide; Demyelinating Diseases; Diabetes Complications; Diabetes Mellitus; Female; Humans; Hypoglycemic Agents; Hyponatremia; Magnetic Resonance Imaging; Male; Middle Aged; Osmolar Concentration; Pons; Vasopressins

Topics: Diabetes Insipidus; Diabetes Mellitus; Diagnosis, Differential; Diuresis; Humans; Hypothalamo-Hypophyseal System; Polyuria; Syndrome; Thirst; Vasopressins

Plasma vasopressin, vasopressin-induced platelet aggregation, and platelet vasopressin receptors were investigated in 10 normal subjects and 14 diabetic patients free of microangiopathy. Basal plasma vasopressin concentration was identical in two groups. Platelet aggregation induced by vasopressin as well as by epinephrine was not significantly altered in the diabetic patients. However, exploration of platelet V1-vasopressin receptors revealed in the diabetic group a dramatic reduction in the number of binding sites without alteration of the receptor affinity for tritiated vasopressin. Thus vasopressin-induced platelet aggregation in uncomplicated diabetes mellitus remains normal despite a decrease in the number of vasopressin receptors presumably due to alterations of the platelet membrane structure.

Topics: Adult; Blood Glucose; Cell Membrane; Diabetes Mellitus; Epinephrine; Female; Humans; Male; Middle Aged; Platelet Aggregation; Receptors, Angiotensin; Receptors, Vasopressin; Vasopressins

Complete cDNA sequences for the vasopressin and oxytocin precursor polyproteins have been determined for the rat, calf, human and pig (vasopressin only), indicating the essential conservation of the precursor structures throughout mammals. DNA probes specific for vasopressin or oxytocin mRNAs have been used to identify both classic (hypothalamic) and novel (thymus, corpus luteum, phaeochromocytoma) sites of hormone expression. Semiquantitative DNA/RNA hybridization suggests that in rats expression of the vasopressin and oxytocin genes is positively effected by osmotic stress, negatively by a systemically applied excess of vasopressin; in the latter experiment a reduction in the hypothalamic levels of vasopressin and oxytocin mRNAs in normal and Brattleboro rats have been observed. This suggests a feedback regulation by the hormone as a possible element in controlling the transcription of the vasopressin gene.

Topics: Animals; Base Sequence; Cattle; Diabetes Mellitus; DNA; Female; Gene Expression Regulation; Humans; In Vitro Techniques; Oxytocin; Rats; RNA, Messenger; Species Specificity; Swine; Vasopressins

Topics: Animals; Blood Volume; Diabetes Mellitus; Glomerular Filtration Rate; Hemodynamics; Kidney; Male; Plasma Volume; Rats; Rats, Brattleboro; Rats, Inbred Strains; Vasopressins; Water-Electrolyte Imbalance

Topics: Diabetes Insipidus; Diabetes Mellitus; Diagnosis, Differential; Female; Humans; Male; Vasopressins

It is very rare for disturbances of water balance to occur as isolated phenomena. More commonly, mixed electrolyte abnormalities present. However, to permit the logical application of therapy an understanding of basic water balance in health and disease is essential.

Topics: Dehydration; Diabetes Insipidus; Diabetes Mellitus; Humans; Osmolar Concentration; Thirst; Vasopressins; Water; Water Intoxication; Water Loss, Insensible; Water-Electrolyte Imbalance

Topics: Adolescent; Adult; Craniopharyngioma; Diabetes Mellitus; Humans; Pituitary Neoplasms; Postoperative Complications; Vasopressins

Plasma vasopressin was measured in seven insulin-treated diabetics during 24 h of insulin withdrawal to determine: 1) if abnormalities of the neurohypophysial-renal axis contribute to the dehydration of uncontrolled diabetes mellitus; and 2) the factors causing elevated levels of vasopressin in diabetic ketoacidosis. During the 24 h period of insulin withdrawal, blood glucose rose from 6.7 +/- 1.0 to 20.7 +/- 2.4 mmol/l, whereas plasma vasopressin was 3.6 +/- 0.5 pg/ml initially and in four patients showed little change. Markedly elevated levels of plasma vasopressin (17.8, 19.8 and 26.6 pg/ml) were observed in three patients following the onset of hypovolaemia, nausea and/or vomiting which are known to stimulate vasopressin release. Free water clearance was negative throughout the study in all patients. Thirst was not noted despite marked hyperglycaemia (16.9 +/- 2.5 mmol/l) until a significant fall in body weight of 0.9 +/- 0.2 kg had occurred (p less than 0.005). We concluded that marked elevation of vasopressin results from non-osmotic stimulation and that the mechanisms of body water conservation are overridden by the glycosuric diuresis.

Topics: Adult; Blood Glucose; Blood Pressure; Body Weight; Diabetes Mellitus; Female; Humans; Insulin; Male; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Imbalance

The paraventricular nucleus of the rat hypothalamus has been shown to project to the medulla and spinal cord. The proportion of oxytocin-neurophysin (OTNP) axons to vasopressin-neurophysin (VPNP) axons in these structures is unknown. A major difficulty in resolving this problem in previous immunocytochemical studies was the lack of a specific antiserum to each rat neurophysin. In this study two approaches have been used: (1) comparison of immunostaining for neurophysin in normal versus homozygous Brattleboro rats with diabetes insipidus (HODI) which lack VPNP, and (2) application of an antiserum to both rat neurophysins absorbed with HODI rat hypothalamic-pituitary extracts which contain only OTNP. The latter would result in an antiserum specific for VPNP. Our results indicate that the axons which constitute the caudal projections from the paraventricular nucleus are predominately oxytocinergic, the vasopressinergic innervation being limited to the nucleus tractus solitarius, the dorsal motor nucleus of vagus, and the substantia gelatinosa. A similar number of reactive fibers were seen in the medulla and spinal cord of normal and HODI rats. No positive perikarya were observed caudal to the hypothalamus. Fibers in the medulla appeared to terminate in the nucleus of the solitary tract and in the dorsal motor nucleus of the vagus nerve. Positive fibers throughout the cord were present in the substantia gelatinosa and in the intermediolateral grey. The possible role(s) of these projections in integrating autonomic functions and afferent information with neuroendocrine regulation is discussed.

Topics: Animals; Axons; Diabetes Insipidus; Diabetes Mellitus; Hypothalamus; Immunoenzyme Techniques; Medulla Oblongata; Neural Pathways; Neurophysins; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Receptors, Cell Surface; Spinal Cord; Staining and Labeling; Vasopressins

An attempt is made to justify the model of the regulation of agonistic-antagonistic hormonal couples (in the field of the adrenal-postpituitary interrelationships). A method of synthesis for these equations is proposed. Cancerous pathology of this regulation could be due to a disturbance in the secretion or in the catabolism of vasopressin.

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Animals; Diabetes Mellitus; Humans; Hypothalamo-Hypophyseal System; Models, Biological; Neoplasms; Pituitary Hormones; Pituitary-Adrenal System; Receptors, Cell Surface; Vasopressins

Topics: Adult; Aged; Blood Glucose; Chlorpropamide; Diabetes Mellitus; Female; Humans; Male; Middle Aged; Sodium; Time Factors; Vasopressins

Topics: Chlorpropamide; Diabetes Mellitus; Humans; Vasopressins

Concentrations of the antidiuretic hormone, arginine vasopressin, were measured in 28 patients with severe hyperglycemia to determine if abnormalities in hormonal regulation of water excretion could contribute to the extreme dehydration of uncontrolled diabetes mellitus. Vasopressin levels were markedly elevated in both nonketotic and ketotic patients, indicating that vasopressin deficiency plays no role in the polyuria that accompanies hyperglycemia. Instead, the observed increases in vasopressin represent an ineffective effort to conserve water in the face of an overwhelming solute diuresis caused by the glucosuria. The reasons for such marked elevations in plasma vasopressin in these diabetic patients are multifactorial. Both groups of diabetic patients had evidence of hypovolemia, which was sufficient in magnitude to stimulate vasopressin release. Furthermore, nausea provided an independent stimulus to vasopressin secretion in many patients. Osmotic stimulation might have resulted from the large fraction of unidentified plasma solutes, but this factor alone was not sufficient to explain the markedly increased concentrations of vasopressin. Whether such elevations in vasopressin could have metabolic and/or hemodynamic effects in uncrontrolled diabetes remains to be established.

Topics: Adolescent; Adult; Aged; Blood; Blood Glucose; Blood Pressure; Diabetes Mellitus; Diabetic Ketoacidosis; Female; Humans; Male; Middle Aged; Osmolar Concentration; Renin; Sodium; Urea; Urine; Vasopressins

Topics: Aged; Chlorpropamide; Diabetes Mellitus; Female; Humans; Male; Middle Aged; Syndrome; Vasopressins

Topics: Angiotensin II; Animals; Diabetes Mellitus; Epinephrine; Fatty Acids, Nonesterified; Glucagon; Glucose; Glycerides; Hormones; Insulin; Liver; Liver Glycogen; Nucleotides, Cyclic; Obesity; Oxytocin; Parathyroid Hormone; Protein Kinases; Starvation; Stress, Physiological; Vasopressins

A few rare syndromes have been delineated in which diabetes mellitus is inherited in association with other conditions. This paper describes five patients, including four siblings in one family, who have diabetes insipidus, diabetes mellitus, optic atrophy and deafness (the DIDMOAD syndrome). The parents of both families are normal but are first cousins. All the patients have insulin-dependent diabetes mellitus with a typical juvenile-onset. The onset of diabetes insipidus was insidious and the symptoms could easily have been ascribed to poor control of diabetes mellitus. The importance of diagnosing diabetes insipidus is that all these patients had dilatation of the urinary tract varying from mild hydroureter to severe hydronephrosis and this improved with treatment of the diabetes insipidus. It is suggested that patients with diabetes mellitus and optic atrophy should have regular screening tests for diabetes insipidus since it is likely that they represent cases of the full syndrome with incomplete clinical expression. The occurrence of this rare syndrome in four siblings of unaffected parents indicates that the syndrome is due to a recessive gene, but the pathogenesis is unknown.

Topics: Adolescent; Adult; Deafness; Diabetes Insipidus; Diabetes Mellitus; Female; Genes, Recessive; Humans; Hydronephrosis; Male; Optic Atrophy; Osmolar Concentration; Pedigree; Syndrome; Urinary Bladder; Urine; Vasopressins; Water Deprivation

Topics: Adolescent; Adult; Arginine; Diabetes Mellitus; Female; Humans; Male; Vasopressins

Topics: Animals; Diabetes Insipidus; Diabetes Mellitus; Drinking Behavior; Female; Heterozygote; Homozygote; Hypothalamus; Male; Oxytocin; Pituitary Gland; Rats; Renin; Sex Factors; Urine; Vasopressins

Three male siblings with diabetes mellitus are described, two of whom also had coexistent diabetes insipidus. The co-existence of diabetes mellitus and insipidus appears to represent a single genetic abnormality and may or may not be accompanied by primary optic atrophy. Chlorpropamide was effective in controlling the symptoms of diabetes mellitus and diabetes insipidus.

Topics: Adult; Chlorpropamide; Diabetes Insipidus; Diabetes Mellitus; Diabetic Retinopathy; Humans; Kidney Concentrating Ability; Male; Middle Aged; Sex Chromosomes; Vasopressins

The mechanism of lithium-induced diabetes insipidus was investigated in 96 patients and in a rat model. Polydipsia was reported by 40% and polyuria (more than 3 liter/day) by 12% of patients receiving lithium. Maximum concentrating ability after dehydration and vasopressin was markedly impaired in 10 polyuric patients and was reduced in 7 of 10 nonpolyuric patients studied before and during lithium therapy. Severe polyuria (more than 6 liter/day) was unresponsive to trials of vasopressin and chlorpropamide, but improved on chlorothiazide. Rats receiving lithium (3-4 meq/kg/day) developed massive polyuria that was resistant to vasopressin, in comparison to rats with comparable polyuria induced by drinking glucose. Analysis of renal tissue in rats with lithium polyuria showed progressive increase in the concentration of lithium from cortex to papilla with a 2.9-fold corticopapillary gradient for lithium. The normal corticopapillary gradient for sodium was not reduced by lithium treatment. The polyuria was not interrupted by brief intravenous doses of vasopressin (5-10 mU/kg) or dibutyryl cyclic AMP (10-15 mg/kg) capable of reversing water diuresis in normal and hypothalamic diabetes insipidus rats (Brattleboro strain). The present studies suggest that nephrogenic diabetes insipidus is a common finding after lithium treatment and results in part from interference with the mediation of vasopressin at a step distal to the formation of 3',5' cyclic AMP.

Topics: Animals; Bucladesine; Chlorothiazide; Chlorpropamide; Diabetes Mellitus; Diuresis; Glomerular Filtration Rate; Humans; Inulin; Kidney; Kidney Concentrating Ability; Lithium; Polyuria; Potassium; Rats; Sodium; Tritium; Vasopressins

Topics: Adolescent; Adult; Blood Glucose; Diabetes Insipidus; Diabetes Mellitus; Fatty Acids, Nonesterified; Female; Glucagon; Glucose Tolerance Test; Growth Hormone; Humans; Hydrocortisone; Insulin; Male; Middle Aged; Tolbutamide; Vasopressins

Topics: Blood Glucose; Diabetes Mellitus; Diuresis; Glomerular Filtration Rate; Glycosuria; Humans; Kidney; Kidney Concentrating Ability; Kidney Function Tests; Kidney Tubules; Osmolar Concentration; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Topics: Blood Glucose; Diabetes Mellitus; Diuresis; Glomerular Filtration Rate; Glycosuria, Renal; Humans; Kidney; Kidney Function Tests; Vasopressins; Water-Electrolyte Balance

Topics: Adrenalectomy; Animals; Diabetes Mellitus; Insulin; Rats; Vasopressins

Topics: Aged; Central Nervous System Diseases; Chlorpropamide; Diabetes Mellitus; Female; Humans; Hyponatremia; Natriuresis; Osmolar Concentration; Syndrome; Time Factors; Urination Disorders; Vasopressins

Topics: Adipose Tissue; Animals; Blood Glucose; Carbon Dioxide; Carbon Isotopes; Cricetinae; Diabetes Mellitus; Dogs; Female; Glucose; Hyperglycemia; Insulin; Male; Oxytocin; Pancreatectomy; Peptides; Pituitary Hormones, Posterior; Rats; Structure-Activity Relationship; Vasopressins; Vasotocin

Topics: Aged; Animals; Cell Membrane Permeability; Chlorpropamide; Cyclic AMP; Diabetes Insipidus; Diabetes Mellitus; Diuresis; Drug Synergism; Humans; Rats; Theophylline; Vasopressins

Topics: Child; Consanguinity; Diabetes Insipidus; Diabetes Mellitus; Diabetes Mellitus, Type 1; Female; Humans; Insulin; Vasopressins

Topics: Aged; Chlorpropamide; Diabetes Mellitus; Female; Humans; Hyponatremia; Kidney Tubules; Male; Tolazamide; Vasopressins; Water Intoxication

Topics: Aged; Blood; Chlorpropamide; Diabetes Mellitus; Diuresis; Female; Humans; Hyponatremia; Kidney Function Tests; Middle Aged; Natriuresis; Osmolar Concentration; Sodium; Vasopressins

Topics: Aged; Atrophy; Blood; Brain Diseases; Chlorpropamide; Diabetes Complications; Diabetes Mellitus; Female; Fludrocortisone; Humans; Hyperpituitarism; Hyponatremia; Natriuresis; Osmolar Concentration; Tolbutamide; Urine; Vasopressins

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Circadian Rhythm; Diabetes Insipidus; Diabetes Mellitus; Female; Humans; Hydrocortisone; Male; Middle Aged; Vasopressins

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; Dehydration; Diabetes Mellitus; Diabetes Mellitus, Experimental; Drinking; Insulin, Long-Acting; Male; Osmolar Concentration; Pancreatectomy; Pituitary Gland, Posterior; Plasma; Rats; Vasopressins; Water

Topics: Acromegaly; Adrenal Glands; Adrenocorticotropic Hormone; Adult; Dexamethasone; Diabetes Mellitus; Dysautonomia, Familial; Dyspepsia; Female; Goiter; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Lysine; Male; Middle Aged; Vasopressins

Topics: Adult; Blood Glucose; Dehydration; Diabetes Mellitus; Diabetic Coma; Diabetic Ketoacidosis; Diabetic Retinopathy; Glucose; Humans; Hyperglycemia; Hypothalamo-Hypophyseal System; Iatrogenic Disease; Insulin; Male; Pituitary Hormones, Anterior; Stress, Physiological; Vasopressins

Topics: Diabetes Insipidus; Diabetes Mellitus; Diuresis; Female; Glomerular Filtration Rate; Humans; Hyperthyroidism; Kidney Diseases; Kidney Tubules; Male; Neurotic Disorders; Polyuria; Thirst; Vasopressins

Topics: Blood Chemical Analysis; Carbon Dioxide; Chlorides; Diabetes Insipidus; Diabetes Mellitus; Glucose Tolerance Test; Glycosuria; Hematuria; Humans; Hydronephrosis; Hyperglycemia; Nitrogen; Polyuria; Potassium; Pseudomonas Infections; Sodium; Urea; Urinary Tract Infections; Urine; Urography; Vasopressins

Topics: Aerosols; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Female; Humans; Hypersensitivity; Lypressin; Lysine; Pregnancy; Pregnancy in Diabetics; Toxicology; Vasopressins; Water Intoxication

Topics: Arginine Vasopressin; Diabetes Mellitus; Hypophysectomy; Hypothalamo-Hypophyseal System; Neurosurgery; Neurosurgical Procedures; Physiology; Pituitary Gland; Pituitary Gland, Posterior; Rats; Research; Vasopressins; Weaning

Topics: Adolescent; Cortisone; Diabetes Mellitus; Diabetes Mellitus, Type 1; Diabetic Angiopathies; Diabetic Retinopathy; Geriatrics; Gonadal Steroid Hormones; Humans; Hypophysectomy; Insulin; Kidney Diseases; Thyroxine; Vasopressins

Topics: Adolescent; Child; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Female; Genetics, Medical; Humans; Siblings; Vasopressins

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Arginine Vasopressin; Blood Glucose; Diabetes Mellitus; Dogs; Hypoglycemic Agents; Hypophysectomy; Insulin; Research; Vasopressins

Topics: Arginine Vasopressin; Calcium; Diabetes Mellitus; Hypercalcemia; Kidney; Permeability; Pharmacology; Rats; Research; Vasopressins

Topics: Acidosis; Antidiuretic Agents; Blood Chemical Analysis; Blood Glucose; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Diabetic Ketoacidosis; Humans; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Diabetes Mellitus; Humans; Vasopressins; Water-Electrolyte Balance

Topics: Cataract; Child; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Eosinophilia; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Toxoplasmosis; Toxoplasmosis, Congenital; Vasopressins

Topics: Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Vasopressins