pituitrin has been researched along with Hyperaldosteronism* in 45 studies
16 review(s) available for pituitrin and Hyperaldosteronism
Article | Year |
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[Secondary hypertension to endocrine diseases and electrolyte imbalance].
Topics: Cushing Syndrome; Edema; Humans; Hyperaldosteronism; Hypertension; Hypokalemia; Hyponatremia; Inappropriate ADH Syndrome; Mineralocorticoid Excess Syndrome, Apparent; Renin-Angiotensin System; Vasopressins | 2006 |
[Vasoactive substances and water-electrolyte metabolism].
Topics: Body Water; Diabetes Insipidus; Electrolytes; Humans; Hyperaldosteronism; Hypertension; Hypoaldosteronism; Inappropriate ADH Syndrome; Natriuretic Peptides; Renin-Angiotensin System; Vasopressins; Water-Electrolyte Imbalance | 2006 |
[Diagnosis of water-electrolyte imbalance by analysis of vasopressin and atrial natriuretic hormone].
Topics: Atrial Natriuretic Factor; Biomarkers; Humans; Hyperaldosteronism; Hypothyroidism; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Balance | 1998 |
Disturbances in salt and water metabolism in hypertension.
Topics: Atrial Natriuretic Factor; Humans; Hyperaldosteronism; Hypertension; Natriuresis; Sodium, Dietary; Vasopressins; Water-Electrolyte Imbalance | 1989 |
[Current status and prospects of the laboratory diagnosis of arterial hypertension].
Topics: Adrenal Gland Neoplasms; Aldosterone; Angiotensin II; Catecholamines; Diagnosis, Differential; Humans; Hyperaldosteronism; Hypertension; Kinins; Natriuretic Agents; Pheochromocytoma; Potassium; Prostaglandins; Renin; Serotonin; Vasopressins | 1986 |
Thirst and vasopressin function in normal and disordered states of water balance.
Topics: Animals; Blood; Blood Pressure; Blood Volume; Diabetes Insipidus; Diuresis; Female; Humans; Hyperaldosteronism; Hypernatremia; Hyponatremia; Hypothalamus; Lung Neoplasms; Nausea; Osmolar Concentration; Pituitary Gland, Posterior; Pregnancy; Pressoreceptors; Sodium; Thirst; Urine; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance | 1983 |
The clinical physiology of water metabolism. Part I: The physiologic regulation of arginine vasopressin secretion and thirst.
Water balance is tightly regulated within a tolerance of less than 1 percent by a physiologic control system located in the hypothalamus. Body water homeostasis is achieved by balancing renal and nonrenal water losses with appropriate water intake. The major stimulus to thirst is increased osmolality of body fluids as perceived by osmoreceptors in the anteroventral hypothalamus. Hypovolemia also has an important effect on thirst which is mediated by arterial baroreceptors and by the renin-angiotensin system. Renal water loss is determined by the circulating level of the antidiuretic hormone, arginine vasopressin (AVP). AVP is synthesized in specialized neurosecretory cells located in the supraoptic and paraventricular nuclei in the hypothalamus and is transported in neurosecretory granules down elongated axons to the posterior pituitary. Depolarization of the neurosecretory neurons results in the exocytosis of the granules and the release of AVP and its carrier protein (neurophysin) into the circulation. AVP is secreted in response to a wide variety of stimuli. Change in body fluid osmolality is the most potent factor affecting AVP secretion, but hypovolemia, the renin-angiotensin system, hypoxia, hypercapnia, hyperthermia and pain also have important effects. Many drugs have been shown to stimulate the release of AVP as well. Small changes in plasma AVP concentration of from 0.5 to 4 muU per ml have major effects on urine osmolality and renal water handling. Topics: Adolescent; Adult; Aged; Animals; Arginine Vasopressin; Blood Volume; Body Fluids; Body Water; Child; Child, Preschool; Dehydration; Diabetes Insipidus; Dogs; Female; Homeostasis; Humans; Hyperaldosteronism; Hypothalamus; Infant; Infant, Newborn; Kidney; Male; Middle Aged; Osmosis; Rats; Sheep; Thirst; Vasopressins; Water-Electrolyte Balance | 1979 |
Prostaglandins, potassium, and Bartter's syndrome.
Topics: Bartter Syndrome; Humans; Hyperaldosteronism; Kidney; Potassium; Prostaglandins; Prostaglandins E; Renin; Vasopressins | 1978 |
Surgery and the adrenal cortex.
Topics: Adrenal Gland Diseases; Adrenal Glands; Adrenalectomy; Cushing Syndrome; Dexamethasone; Diagnosis, Differential; Humans; Hydrocortisone; Hyperaldosteronism; Hypertension; Hypokalemia; Kidney; Obesity; Pituitary-Adrenal Function Tests; Pituitary-Adrenal System; Vasopressins | 1974 |
The physiology of renin.
Topics: Aldosterone; Angiotensin II; Edema; Extracellular Space; Female; Glomerular Filtration Rate; Humans; Hyperaldosteronism; Hypertension; Hypotension; Juxtaglomerular Apparatus; Kidney; Kidney Diseases; Kidney Failure, Chronic; Natriuresis; Potassium; Pregnancy; Pregnancy Complications; Pressoreceptors; Regional Blood Flow; Renal Artery Obstruction; Renin; Vasopressins | 1973 |
[Ectopic paraneoplastic endocrinopathies associated with water-electrolyte balance disorders].
Topics: Adolescent; Bronchial Neoplasms; Carcinoma, Small Cell; Child, Preschool; Cushing Syndrome; Diagnosis, Differential; Hormones, Ectopic; Humans; Hyperaldosteronism; Hypercalcemia; Hyperparathyroidism; Hyponatremia; Kidney Neoplasms; Paraneoplastic Endocrine Syndromes; Renin; Sodium Chloride; Syndrome; Vasopressins | 1973 |
[Liver cirrhosis. 3. Advances in treatment].
Topics: Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hyperaldosteronism; Liver Cirrhosis; Potassium; Rest; Sodium; Vasopressins; Vitamins | 1973 |
[Role of hormones in magnesium metabolism].
Topics: Addison Disease; Animals; Calcitonin; Glucocorticoids; Growth Hormone; Hormones; Humans; Hyperaldosteronism; Hyperparathyroidism; Hyperthyroidism; Hypoparathyroidism; Insulin; Intestinal Absorption; Magnesium; Parathyroid Hormone; Rats; Vasopressins; Vitamin D | 1969 |
[Diabetes insipidus].
Topics: Adolescent; Adult; Aged; Animals; Arginine; Child; Dehydration; Diabetes Insipidus; Female; Humans; Hyperaldosteronism; Hypertonic Solutions; Hypocalcemia; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules; Male; Middle Aged; Nicotine; Osmolar Concentration; Polyuria; Sex Factors; Sodium Chloride; Thirst; Time Factors; Urine; Urologic Diseases; Vasopressins; Water-Electrolyte Balance | 1969 |
[Endocrine disorders and water metabolism].
Topics: Acromegaly; Addison Disease; Adrenocortical Hyperfunction; Cushing Syndrome; Diabetes Insipidus; Endocrine System Diseases; Humans; Hyperaldosteronism; Hyperparathyroidism; Hypopituitarism; Hypothyroidism; Kidney; Vasopressins; Water-Electrolyte Balance | 1967 |
[Collective review of endocrine factors in various types of cardio-circulatory insufficiency].
Topics: Adrenal Glands; Adrenal Medulla; Edema; Endocrine Glands; Heart; Heart Failure; Humans; Hyperaldosteronism; Shock; Thyroxine; Vasopressins | 1967 |
1 trial(s) available for pituitrin and Hyperaldosteronism
Article | Year |
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Evidence for a role of vasopressin in the control of aldosterone secretion in primary aldosteronism: in vitro and in vivo studies.
Arginine vasopressin (AVP) stimulates steroid secretion from the normal human adrenal gland and some cortisol-producing adrenocortical tumors or hyperplasia through activation of the V(1a) receptor.. The objective of the study was to investigate in vitro and in vivo the possible involvement of AVP in the physiopathology of primary aldosteronism.. The design of the study included immunohistochemical, pharmacological, and molecular studies on aldosterone-producing adenoma (APA), followed by a monocentric, crossover trial of the orally active V(1a) receptor antagonist, SR 49059, in a double blind, randomized, and placebo-controlled fashion.. The study was conducted at a university hospital and research laboratory.. The study population included eight untreated patients with primary aldosteronism, four with APA and four with idiopathic hyperaldosteronism.. Aldosterone secretion of APA cells in vitro and plasma aldosterone, renin, and ACTH were measured.. SR 49059 (200 mg once daily) or placebo was administered during two 1-wk treatment periods separated by a 2-wk washout.. We observed the occurrence of AVP-containing cells in APA tissues. Administration of AVP to perifused APA cells induced an increase in aldosterone production, which was inhibited by a specific V(1a) antagonist. RT-PCR analysis showed the expression of V(1a) receptor mRNA in most APAs studied. In APA patients, SR 49059 did not induce any effect on basal aldosterone secretion but provoked a plasma aldosterone response to orthostatism (P < 0.03) and strengthened the positive correlation between plasma aldosterone and ACTH.. The present study indicates that functional V(1a) receptors are present in APA and suggests that AVP may exert an autocrine/paracrine control of aldosterone secretion in APA tissues. Topics: Adenoma; Adrenocorticotropic Hormone; Aldosterone; Cross-Over Studies; Double-Blind Method; Female; Fluorescent Antibody Technique; Hormone Antagonists; Humans; Hyperaldosteronism; Immunohistochemistry; Indoles; Male; Middle Aged; Pituitary Neoplasms; Pyrrolidines; Receptors, Vasopressin; Reverse Transcriptase Polymerase Chain Reaction; RNA; Vasopressins | 2006 |
28 other study(ies) available for pituitrin and Hyperaldosteronism
Article | Year |
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Partial vasopressin 1a receptor agonism reduces portal hypertension and hyperaldosteronism and induces a powerful diuretic and natriuretic effect in rats with cirrhosis and ascites.
The vasopressin system has emerged as a therapeutic focus for lowering portal hypertension and reducing splanchnic vasodilation in patients with refractory ascites. Clinically available vasopressin agonists are limited by preferential selectivity for V1 receptors that also have steep concentration-response curves with potential risks of excess vasoconstriction and/or complete antidiuretic effects. OCE-205 is a novel, selective, partial V1a receptor agonist with mixed agonist/antagonist activity and no V2 receptor activation at therapeutic doses. We carried out two studies assessing the in vivo effects of OCE-205 in different rat models of cirrhosis and ascites. In a carbon tetrachloride rat cirrhosis model, OCE-205 administration produced a marked reduction in portal hypertension and hyperaldosteronism, along with robust diuretic and natriuretic effects. These effects were accompanied by marked decreases in ascites volume, with three of five animals experiencing total mobilization of ascites. There was no evidence of fluid overload or sodium or water retention, confirming OCE-205's lack of V2 receptor activity. In a second, corroborative study using a bile duct ligation rat model of ascites, OCE-205 produced significant decreases in ascites volume and body weight and a significant increase in urine volume versus vehicle. Urine sodium excretion increased significantly after the first administration of OCE-205 relative to vehicle; however, repeat administration over 5 days did not lead to hyponatremia. Thus, in separate in vivo models, the mixed agonist/antagonist OCE-205 demonstrated relevant and expected endpoint findings consistent with its known mechanism of action and in vitro pharmacology without apparent unwanted effects or nonspecific toxicities. Topics: Animals; Ascites; Diuretics; Hyperaldosteronism; Hypertension, Portal; Liver Cirrhosis; Natriuretic Agents; Rats; Receptors, Vasopressin; Sodium; Vasopressins | 2023 |
Hyperaldosteronism in Klotho-deficient mice.
Klotho is a membrane protein participating in the inhibitory effect of FGF23 on the formation of 1,25-dihydroxyvitamin-D(3) [1,25(OH)(2)D(3)]. It participates in the regulation of renal tubular phosphate reabsorption and stimulates renal tubular Ca(2+) reabsorption. Klotho hypomorphic mice (klotho(hm)) suffer from severe growth deficit, rapid aging, and early death, events largely reversed by a vitamin D-deficient diet. The present study explored the role of Klotho deficiency in mineral and electrolyte metabolism. To this end, klotho(hm) mice and wild-type mice (klotho(+/+)) were subjected to a normal (D(+)) or vitamin D-deficient (D(-)) diet or to a vitamin D-deficient diet for 4 wk and then to a normal diet (D(-/+)). At the age of 8 wk, body weight was significantly lower in klotho(hm)D(+) mice than in klotho(+/+)D(+) mice, klotho(hm)D(-) mice, and klotho(hm)D(-/+) mice. Plasma concentrations of 1,25(OH)(2)D(3,) adrenocorticotropic hormone (ACTH), antidiuretic hormone (ADH), and aldosterone were significantly higher in klotho(hm)D(+) mice than in klotho(+/+)D(+) mice. Plasma volume was significantly smaller in klotho(hm)D(-/+) mice, and plasma urea, Ca(2+), phosphate and Na(+), but not K(+) concentrations were significantly higher in klotho(hm)D(+) mice than in klotho(+/+)D(+) mice. The differences were partially abrogated by a vitamin D-deficient diet. Moreover, the hyperaldosteronism was partially reversed by Ca(2+)-deficient diet. Ussing chamber experiments revealed a marked increase in amiloride-sensitive current across the colonic epithelium, pointing to enhanced epithelial sodium channel (ENaC) activity. A salt-deficient diet tended to decrease and a salt-rich diet significantly increased the life span of klotho(hm)D(+) mice. In conclusion, the present observation disclose that the excessive formation of 1,25(OH)(2)D(3) in Klotho-deficient mice results in extracellular volume depletion, which significantly contributes to the shortening of life span. Topics: Adrenocorticotropic Hormone; Aldosterone; Animals; Blood Chemical Analysis; Blood Pressure; Body Weight; Calcitriol; Diffusion Chambers, Culture; Electrolytes; Fibroblast Growth Factor-23; Glucuronidase; Hyperaldosteronism; Klotho Proteins; Mice; Mice, Knockout; Parathyroid Hormone; Plasma Volume; Survival; Vasopressins | 2010 |
Maternal pseudo primary hyperaldosteronism in twin-to-twin transfusion syndrome.
To monitor changes in the maternal renin-angiotensin-aldosterone system following laser therapy and amnioreduction in severe twin-to-twin transfusion syndrome (TTTS).. Observational prospective study.. Single university hospital in Poissy, France.. Sixty cases of TTTS at 16-26 weeks of gestation.. Maternal blood sampling before, 6 and 24 hours following the procedure.. Plasma levels of aldosterone, renin, angiotensin II (AII), atrial natriuretic peptide (ANP), vasopressin, sodium, potassium and plasma proteins together with full blood count were measured before, 6 and 24 hours following the procedure.. TTTS is associated with maternal hyperaldosteronism dissociated from renin-angiotensin changes. Correcting TTTS by placental surgery and amnioreduction triggers incomplete correction of hyperaldosteronism, as early as 6 hours following the procedure, without changes in AII but an increase in the levels of ANP in plasma. Electrolyte concentrations remained stable despite haemodilution, while vasoactive hormone levels such as that of vasopressin remained unchanged.. Mechanisms involved in marked fluid retention in TTTS are rapidly corrected by laser therapy followed by amnioreduction while maintaining electrolyte homeostasis. Topics: Adult; Analysis of Variance; Atrial Natriuretic Factor; Female; Fetofetal Transfusion; Hematocrit; Hemoglobins; Humans; Hyperaldosteronism; Laser Therapy; Plasma Substitutes; Pregnancy; Pregnancy Complications; Pregnancy Reduction, Multifetal; Pregnancy Trimester, Second; Pregnancy, Multiple; Renin; Vasopressins | 2007 |
Increased renal alpha-ENaC and NCC abundance and elevated blood pressure are independent of hyperaldosteronism in vasopressin escape.
Previously, we demonstrated that rats undergoing vasopressin escape had increased mean arterial blood pressure (MAP), plasma and urine aldosterone, and increased renal protein abundance of the alpha-subunit of the epithelial sodium channel (ENaC), the thiazide-sensitive Na-Cl cotransporter (NCC), and the 70-kDa band of gamma-ENaC (Song J, Hu X, Khan O, Tian Y, Verbalis JG, and Ecelbarger CA. Am J Physiol Renal Physiol 287: F1076-F1083, 2004; Ecelbarger CA, Knepper MA, and Verbalis JG. J Am Soc Nephrol 12: 207-217, 2001). Here, we determine whether changes in these renal proteins and MAP require elevated aldosterone levels. We performed adrenalectomies (ADX) or sham surgeries on male Sprague-Dawley rats. Corticosterone and aldosterone were replaced to clamp these hormone levels. MAP was monitored by radiotelemetry. Rats were infused with 1-deamino-[8-D-arginine]-vasopressin (dDAVP) via osmotic minipumps (5 ng/h). At day 3 of dDAVP infusion, seven rats in each group were offered a liquid diet [water load (WL)] or continued on a solid diet (SD). Plasma aldosterone and corticosterone and urine aldosterone were increased by WL in sham rats. ADX-WL rats escaped, as assessed by early natriuresis followed by diuresis; however, urine volume and natriuresis were somewhat blunted. WL did not reduce the abundance or activity of 11-beta-hydroxsteroid dehydrogenase type 2. Furthermore, the previously observed increase in renal aldosterone-sensitive proteins and escape-associated increased MAP persisted in clamped rats. The densitometry of immunoblots for NCC, alpha- and gamma-70 kDa ENaC, respectively, were (% sham-SD): sham-WL, 159, 278, 233; ADX-SD, 69, 212, 171; ADX-WL, 116, 302, 161. However, clamping corticosteroids blunted the rise at least for NCC and gamma-ENaC (70 kDa). Overall, the increase in aldosterone observed in vasopressin escape is not necessary for the increased expression of NCC, alpha- or gamma-ENaC or increased MAP associated with "escape." Topics: 11-beta-Hydroxysteroid Dehydrogenase Type 2; Adrenalectomy; Aldosterone; Animals; Blood Pressure; Corticosterone; Deamino Arginine Vasopressin; Diuresis; Drinking; Epithelial Sodium Channels; Gene Expression Regulation; Glomerular Filtration Rate; Hyperaldosteronism; Hypertension; Kidney Tubules, Collecting; Male; Natriuresis; Rats; Rats, Sprague-Dawley; Sodium Channels; Sodium Chloride Symporters; Vasopressins | 2006 |
Aldosteronoma in a dog with polyuria as the leading symptom.
In a 10-year-old castrated male shorthaired German pointer polyuria was associated with slight hypokalemia, hypophosphatemia and alkalosis, as well as elevated plasma concentrations of a glucocorticoid-inducible iso-enzyme of alkaline phosphatase. Repeated measurements of urinary corticoids and normal suppressibility of the hypothalamus-pituitary-adrenocorticial axis excluded glucocorticoid excess. Urine osmolality (Uosm) did not increase during administration of the vasopressin analogue desmopressin. At the time water deprivation had caused Uosm to rise from 300 to 788 mOsm/kg, there was also plasma hypertonicity. During hypertonic saline infusion the osmotic threshold for vasopressin release was increased. The combination of elevated plasma aldosterone concentrations and unmeasurably low plasma renin activity pointed to primary hyperaldosteronism. As initially computed tomography (CT) did not reveal an adrenocortical lesion, the dog was treated with the aldosterone antagonist spironolactone. This caused Uosm to rise in a dose-dependent manner. However, well-concentrated urine was only achieved with doses that gave rise to adverse effects. Once repeated CT, using 2-mm-thick slices, had revealed a small nodule in the cranial pole of the left adrenal, unilateral adrenalectomy was performed which resolved the polyuria completely. Also the plasma concentrations of kalium, aldosterone and renin activity returned to within their respective reference ranges. The adrenocortical nodule had the histological characteristics of an aldosteronoma, with the non-affected zona glomerulosa being atrophic.In this dog with primary hyperaldosteronism the polyuria was characterized by vasopressin resistance and increased osmotic threshold of vasopressin release, similar to the polyuria of glucocorticoid excess. The possibility is discussed that the polyuria of glucocorticoid excess is actually a mineralocorticoid effect. Topics: Adrenalectomy; Aldosterone; Animals; Dog Diseases; Dogs; Hyperaldosteronism; Male; Osmolar Concentration; Polyuria; Renin; Saline Solution, Hypertonic; Urine; Vasopressins | 2001 |
Impaired vasopressin suppression and enhanced atrial natriuretic hormone release following an acute water load in primary aldosteronism.
The release of arginine vasopressin (AVP) and atrial natriuretic hormone (ANH) and their involvement in renal water and electrolyte metabolism in primary aldosteronism in humans were studied. An oral acute water load (20 ml/kg body weight) was given to each of 12 patients before and after surgical removal of their aldosterone-producing adenoma(s). Plasma AVP and ANH were measured simultaneously, and renal water and electrolyte metabolism and tubular functions were determined. The same water load was given to seven normal subjects and the same parameters were determined. In the presence of mineralocorticoid excess before the operation, plasma AVP was relatively low compared with plasma osmolality (Posm), but was not suppressed in response to decreases in Posm after the water load. Baseline plasma ANH was high and increased further after the water load; urinary dilution and diuresis both remained normal. After the operation, baseline plasma AVP was normal and decreased in response to the decrease in Posm after the water load, with normal urinary dilution and diuresis. Baseline plasma ANH was normal, and did not increase after the water load. The ratio of urinary K and Na clearances and distal tubular reabsorption of Na increased before the operation. These results suggest that there are perturbations of AVP and ANH release in primary aldosteronism, despite the normal urinary dilution after a water load. Topics: Adenoma; Adrenal Gland Neoplasms; Adrenalectomy; Adult; Aged; Arginine Vasopressin; Atrial Natriuretic Factor; Blood; Drinking; Female; Humans; Hyperaldosteronism; Male; Middle Aged; Natriuresis; Osmolar Concentration; Postoperative Period; Potassium; Time Factors; Urine; Vasopressins | 1997 |
Development of polyuria in Tsukuba hypertensive mice carrying human renin and angiotensinogen genes.
1. Tsukuba hypertensive mice (THM) carry both human renin and angiotensinogen genes, and develop hypertension. The animal has high levels of renin activity and angiotensin II concentration in the plasma. 2. Urinary excretion in THM was greater than in the control animal, non-transgenic C57BL/6j. THM showed a greater amount of daily water intake. The osmolality of 24 h urine was lower than that of the control animal. 3. When water was deprived for 12 h and then loaded with 0.25 mL/10 g bodyweight, the osmolality of urine at the first 0-3 h period was the same in THM and control, but significantly lower in THM at the following 3-6 h period, indicating that the urine concentrating activity is insufficient in THM compared with the control animal. 4. Urinary excretion of vasopressin was significantly higher in THM. Plasma aldosterone concentration and urinary excretion of aldosterone were also higher in THM. Plasma potassium level was significantly low. 5. The mechanism underlying the pathophysiology of polyuria is not totally explained; however, hypokalaemia, which was probably the result of hyperaldosteronism, may be at least partially involved, since hypokalaemia is considered to be a factor hampering the action of vasopressin for concentration of urine at the site of the collecting duct of the kidney. Topics: Aldosterone; Angiotensinogen; Animals; Electrolytes; Humans; Hyperaldosteronism; Hypertension; Kidney Concentrating Ability; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Polyuria; Rats; Renin; Vasopressins | 1995 |
The CSF aldosterone in brain tumors with brain edema.
The study of renin-angiotensin-aldosterone (RAA) and vasopressin (VP) systems in neurosurgical patients with brain tumors and brain edema (BE) had revealed an excessive activity of these systems with secondary hyperaldosteronism especially with BE that proves the pathogenetic role of these systems. Measurement of Aldosterone (Ald) in CSF may serve as a diagnostic test to help manage the patient's clinical condition. Mechanisms of Ald penetration in CSF assumed to be the result of blood-brain-barrier (BBB) destruction (especially in astrocytomas) and/or the mediation by neuropeptides (for example increasing activity of VP V1-receptors). Results serve as a basis for application of the neuropeptide and hormone antagonists and inhibitors on all stages of cascade reactions taking part in the water and sodium retention. Topics: Adolescent; Adult; Aged; Aldosterone; Astrocytoma; Blood-Brain Barrier; Brain Edema; Brain Neoplasms; Cerebral Hemorrhage; Child; Child, Preschool; Female; Heart Arrest; Hemodynamics; Humans; Hyperaldosteronism; Hypertension; Male; Middle Aged; Postoperative Complications; Prognosis; Radioimmunoassay; Renin-Angiotensin System; Tachycardia; Vasopressins | 1994 |
[Effect of isolated ultrafiltration on plasma hormone levels in patients with heart failure resistant to drug therapy].
The positive action exerted by isolated ultrafiltration on 69 patients with refractory heart failure was shown to be due to the complex interaction of effects produced by ultrafiltrate removal. Among the effects, a leading role is played by therapy for hyperaldosteronism and reduction of antidiuretic hormone levels along with improvement of the functional status of the liver and heart. Topics: Adult; Aged; Aldosterone; Drug Resistance; Female; Heart Failure; Hemofiltration; Humans; Hyperaldosteronism; Male; Middle Aged; Renin; Vasopressins | 1989 |
Mechanisms responsible for thirst and polyuria associated with primary hyperaldosteronism.
Topics: Adult; Diabetes Insipidus; Humans; Hyperaldosteronism; Male; Polyuria; Thirst; Vasopressins | 1987 |
The renal kallikrein-kinin system: a look at the controversies.
Topics: Aldosterone; Animals; Body Water; Humans; Hyperaldosteronism; Kallikreins; Kidney; Kinins; Renal Circulation; Vasopressins | 1986 |
Relation of blood pressure with body and plasma electrolytes in Conn's syndrome.
Thirty-four patients with untreated Conn's syndrome were studied in a metabolic ward. The final diagnosis in each case was based on the finding and removal of an adrenal cortical adenoma with histological features typical of the disorder. Compared with 34 age and sex-matched normal controls the untreated patients had increased plasma aldosterone concentration, increased blood pressure (183/112 mmHg), increased exchangeable sodium (116.7% of normal), hypokalaemia and increased plasma sodium concentration. Exchangeable potassium was lower than normal and plasma concentrations of active renin, total renin and angiotensin II were lower than normal mean values. Arterial pressure correlated significantly and positively with plasma and exchangeable sodium and there was a significant negative correlation with plasma potassium concentration. Partial regression analysis showed that the relation of exchangeable sodium with blood pressure did not depend on age or renal function but that the relation of blood pressure and plasma potassium could be attributed to the correlation of exchangeable sodium and blood pressure. Multiple regression analysis suggested that exchangeable and plasma sodium were the most important determinants of blood pressure in untreated patients. Spironolactone, amiloride and surgical removal of the adenoma corrected the electrolyte abnormality and usually lowered blood pressure. The fall in exchangeable sodium was related to the fall in blood pressure. The pattern of correlation found by multiple regression analysis in postoperative patients was similar to that in normal subjects. The findings are relevant to some of the mechanisms proposed for the hypertension of mineralocorticoid excess. Topics: Adult; Aldosterone; Blood Pressure; Electrolytes; Female; Humans; Hyperaldosteronism; Hypertension; Male; Middle Aged; Mineralocorticoids; Regression Analysis; Sodium; Vasoconstriction; Vasopressins | 1983 |
Pharmacologic studies in Bartter's syndrome: effect of DDAVP and indomethacin on renal concentrating operation. Part II.
We have investigated the effect of indomethacin and DDAVP on water excretion in a patient with familial Bartter's syndrome in whom urinary concentration was impaired during ad libitum fluid intake without any decrease in maximal concentrating ability. In response to indomethacin urine osmolality and free water reabsorption increased, simultaneously with the decrease in the excretion of prostaglandin E2. The indomethacin induced improvement was however less than that obtained after DDAVP with or without indomethacin. The results can be interpreted on the basis of either a direct "vasopressin-like" action of indomethacin or abolishment of the peripheral vasopressin--prostaglandin interaction. The clinical implication is that the theoretical possibility of indomethacin-induced inappropriate ADH syndrome should be borne in mind when a patient is treated with this drug on a long term basis. Topics: Adult; Bartter Syndrome; Deamino Arginine Vasopressin; Diuresis; Humans; Hyperaldosteronism; Indomethacin; Kidney; Male; Osmolar Concentration; Prostaglandins; Vasopressins; Water Deprivation | 1978 |
Blood volume.
During the past decade the diagnostic use of blood volume determinations has declined as a result of the generation of largely inaccurate results and inappropriate normalization and interpretation. After historical development of more than 50 years, current methodology employs 125I-labeled human serum albumin and 51Cr-labeled red blood cells to determine plasma volume and red cell volume, respectively. Accurate blood volume determinations require (1) abandoning the use of the mean body hematocrit:venous hematocrit ratio and using simultaneous independent measurements of both volumes; (2) delaying multiple postinjection patient samples until complete mixing and equilibration are complete; (3) backextrapolation of plasma concentrations of 125I to account for albumin loss from the plasma, and, rarely, back-extrapolation of red cell concentrations to account for dilution by red cells transfused during the procedure; (4) normalization of volumes by adjusting patient weight to normal correspondence with lean tissue mass, whenever necessary. A rapid, routine method that fulfills these four requirements is presented. A number of surgical and medical conditions in which blood volume determinations are very useful in diagnosis and therapy are discussed. Recently developed techniques for blood volume measurements include neutron acativation analysis and fluorescent excitation analysis. Correct normalization of accurate blood volume measurements will provide a valuable service to the entire medical community. Topics: Aged; Blood Volume Determination; Body Constitution; Carbon Monoxide; Central Venous Pressure; Chromium Radioisotopes; Diagnostic Errors; Erythrocytes; Hematocrit; Hormones, Ectopic; Humans; Hyperaldosteronism; Hypertension; Indium; Iron Radioisotopes; Male; Phosphorus Radioisotopes; Plasma Volume; Polycythemia; Postoperative Complications; Potassium Radioisotopes; Radioisotope Dilution Technique; Serum Albumin, Radio-Iodinated; Shock; Technetium; Time Factors; Transferrin; Vasopressins | 1975 |
[Changes in the kidney concentration capacity in patients with primary hyperaldosteronism depending on therapy (author's transl)].
Topics: Glomerular Filtration Rate; Humans; Hyperaldosteronism; Kidney Concentrating Ability; Osmolar Concentration; Vasopressins | 1975 |
Six year follow-up of a child with Bartter syndrome.
Topics: Aldosterone; Alkalosis; Angiotensin II; Biopsy; Blood Pressure; Child, Preschool; Diet Therapy; Female; Follow-Up Studies; Growth Disorders; Humans; Hyperaldosteronism; Hyperplasia; Hypertrophy; Hypokalemia; Juxtaglomerular Apparatus; Kidney Concentrating Ability; Kidney Diseases; Norepinephrine; Potassium; Renin; Secretory Rate; Sodium Chloride; Spironolactone; Syndrome; Vasopressins | 1973 |
[Physiopathology of water-electrolyte disorders in cardiac insufficiency].
Topics: Aldosterone; Catecholamines; Heart Failure; Hemodynamics; Humans; Hyperaldosteronism; Hypokalemia; Hyponatremia; Kidney; Potassium; Renin; Sodium; Vasopressins; Water; Water-Electrolyte Balance | 1973 |
[Investigations of antidiuretic activity in liver cirrhosis].
Topics: Aged; Diuresis; Female; Humans; Hyperaldosteronism; Liver Cirrhosis; Male; Middle Aged; Natriuresis; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Balance | 1973 |
[Renin-angiotensin-adiuretin system].
Topics: Addison Disease; Angiotensin II; Feedback; Humans; Hyperaldosteronism; Renin; Sodium; Vasopressins; Water-Electrolyte Balance | 1972 |
Edema and endocrine disorders.
Topics: Acromegaly; Edema; Endocrine System Diseases; Humans; Hyperaldosteronism; Hyperthyroidism; Hyponatremia; Hypothyroidism; Syndrome; Vasopressins | 1972 |
Responses of plasma LH to insulin-induced hypoglycemia, basopressin, premarin and clomiphene.
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 | 1971 |
[Idiopathic edemas with secondary hyperaldosteronism. Definition, history, pathogenesis].
Topics: Adult; Age Factors; Aldosterone; Body Weight; Capillary Permeability; Edema; Female; Humans; Hyperaldosteronism; Male; Middle Aged; Mineralocorticoid Receptor Antagonists; Natriuresis; Posture; Renin; Sex Factors; Sodium; Vasopressins; Water-Electrolyte Balance | 1970 |
In vitro synthesis of vasopressin by lung tumor cells.
Topics: Carbon Isotopes; Carcinoma, Bronchogenic; Humans; Hyperaldosteronism; Leucine; Lung Neoplasms; Male; Middle Aged; Radioimmunoassay; Tritium; Tyrosine; Vasopressins | 1969 |
[Diuretics in cirrhosis. Accidents. Indications].
Topics: Adrenal Cortex Hormones; Alkalosis; Blood Urea Nitrogen; Blood Volume; Diuretics; Edema; Ethacrynic Acid; Furosemide; Glomerular Filtration Rate; Humans; Hyperaldosteronism; Hyperkalemia; Hypokalemia; Hyponatremia; Kidney Failure, Chronic; Kidney Tubules; Liver Cirrhosis; Spironolactone; Triamterene; Vasopressins | 1969 |
The role of adrenocorticoids in the inappropriate antidiuretic hormone syndrome.
Topics: Adult; Aged; Animals; Biological Assay; Blood Chemical Analysis; Blood Urea Nitrogen; Bronchial Neoplasms; Creatinine; Dexamethasone; Diuresis; Female; Fludrocortisone; Humans; Hyperaldosteronism; Hyponatremia; Male; Middle Aged; Natriuresis; Phenytoin; Rats; Tissue Extracts; Urine; Vasopressins; Water-Electrolyte Balance | 1968 |
Effect of dehydration on plasma renin activity.
Topics: Adolescent; Adult; Blood Volume; Dehydration; Diabetes Insipidus; Female; Hematocrit; Humans; Hyperaldosteronism; Hypertension, Renal; Male; Renin; Sodium; Vasopressins; Water | 1967 |
[THE SYNDROME OF PREMENSTRUAL TENSION. ETIOPATHOGENESIS AND TREATMENT].
Topics: Anti-Allergic Agents; Arginine Vasopressin; Biomedical Research; Estrogens; Female; Histamine H1 Antagonists; Humans; Hyperaldosteronism; Hypernatremia; Premenstrual Syndrome; Progesterone; Progestins; Toxicology; Vasopressins; Water-Electrolyte Balance | 1964 |
Action of antidiuretic hormone in potassium-depleted rats; relation to aldosteronism.
Topics: Aldosterone; Animals; Hyperaldosteronism; Hypokalemia; Potassium; Potassium Deficiency; Rats; Vasopressins | 1958 |