Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polyuria may result from either a water or a solute diuresis. Although the history and physical examination may provide clues to the cause of the polyuria, the definitive diagnosis requires laboratory tests which focus on the osmolality of the urine and serum in combination with the urine volume and the rate of excretion of osmoles. An isoosmolar or hyperosmolar urine is found in children with a solute diuresis or in normal children, whereas a hypoosmolar urine is found in children with a water diuresis. In the latter case, a low serum osmolality suggests primary polydipsia whereas a high serum osmolality suggests antidiuretic hormone (ADH) deficiency or insensitivity. A water deprivation test is necessary when the initial evaluation fails to establish the cause of polyuria. A vasopressin test enables the differentiation between neurogenic and nephrogenic diabetes insipidus (DI).
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PMID:Polyuria in childhood. 174 78

Two pregnant women developed overt polyuria (up to 11 l/day) and polydipsia during their second and third trimesters of pregnancy. In one patient hydronephrosis was present. Both patients suffered from mild gestational diabetes mellitus. Plasma sodium was 145 and 162 mmol/l. Polyuria and urinary hypo-osmolality responded well to desmopressin acetate. After delivery, polyuria and polydipsia disappeared in one patient and significantly improved in the other. Infusion of hypertonic saline one and two weeks respectively after delivery led to plasma hyper-osmolality (294 mosmol/kg and 305 mosmol/kg) without detectable stimulation of arginine vasopressin (AVP). Anterior pituitary function was normal. No stimulation of AVP occurred following insulin-induced hypoglycemia. AVP plasma disappearance after i.v. pulse injection of 1 microgram AVP as well as AVP plasma concentration after continuous infusion of 10 ng AVP/min was studied two weeks after delivery in one patient. The results suggested markedly elevated degradation of AVP compared to control subjects, probably due to an increased vasopressin activity. Eight months after delivery, hypertonic saline infusion in one patient led to a plasma-osmolality of 312 mosmol/kg without stimulation of AVP. In the second patient, AVP was not detectable (less than 0.2 pg/ml) six months after delivery when plasma osmolality was 290 mosmol/kg. Our studies demonstrate that a subclinical compensated diabetes insipidus was preexistent in both patients. Exacerbation occurred due to an increased AVP-clearance and presumably due to the hemodynamic and hormonal alterations during pregnancy, including a mild gestational diabetes mellitus.
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PMID:[Transient polyuria in pregnancy in diabetes insipidus and gestational diabetes]. 177 Sep 4

The antitumor drug celiptium (N2-methyl-9-hydroxyellipticinium) is an ellipticine derivative effective in experimental tumors and in man. The major side effect is nephrotoxicity. The impairment of renal function is studied in rats following a single i.v. dose of 20 mg/kg celiptium and a long-term study (day 2 to day 60). A loss of body weight is noted in celiptium-treated animals between day 4 and day 15, and recovery occurs between day 15 and day 60. Histologic study shows cortical lesions characterized by focal necrosis of proximal tubules without any glomerular, interstitial, and vascular alterations on day 8. It is to be noted that any medullary lesions were not shown. A polyuria and a decreased creatinine clearance are reported on day 8. We were interested in a special study of this polyuria. For this study, rats were water deprived between day 6 and day 8 following celiptium administration. The decrease of urinary osmolality is not recovered after dehydration and exogenous vasopressin derivative (dD AVP) does not correct the renal concentration defect. AVP plasma levels increase after dehydration. These results suggest a pitressino-resistant urinary concentrating inability in celiptium-treated rats.
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PMID:Nephrotoxicity of an ellipticine derivative (N2-methyl-9-hydroxyellipticinium acetate) in rat: a defect of urinary concentrating ability. 178 Apr 92

Supraventricular tachycardia was induced in 10 patients by programmed cardiac stimulation through esophageal lead. Blood pressure, heart rate, renal function, and hormonal factors were measured before, during, and after tachycardia. The patients were divided into two groups, depending on whether antinatriuresis occurred during tachycardia; one group (n = 5) with antinatriuresis during tachycardia associated with a decrease in blood pressure and the other group (n = 5) with neither antinatriuresis nor changes in blood pressure. The urinary sodium excretion tended to increase after tachycardia only in the latter group. On the other hand, urine volume and free water clearance increased during or after tachycardia in both groups. Plasma levels of atrial natriuretic peptide significantly increased and the urinary vasopressin excretion significantly decreased during tachycardia in both groups. During tachycardia, natriuresis due to atrial natriuretic peptide secretion seems to be hampered by hypotension, but polyuria is preserved despite the fall in blood pressure probably related to suppression of vasopressin release.
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PMID:Dominance of blood pressure in natriuresis associated with supraventricular tachycardia. 182 64

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.
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PMID:Different mechanisms of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia. 183 Apr 49

Shortly after diagnosis of primary hyperparathyroidism, a patient had serum hyperosmolality, polyuria, isosthenuria, profound potassium depletion, and elevated plasma antidiuretic hormone levels, all consistent with nephrogenic diabetes insipidus. After parathyroidectomy, serum calcium and serum osmolality levels fell concurrently. Profound potassium deficits did not recur. We propose that (1) hypercalcemia produced a concentrating defect and polyuria; (2) renal tubular acidosis and polyuria combined to produce severe potassium depletion; (3) hypokalemia potentiated the nephrogenic diabetes insipidus caused by hypercalcemia; and (4) postoperative disappearance of the diabetes insipidus confirmed its reversible, purely metabolic causes.
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PMID:Primary hyperparathyroidism and coexisting nephrogenic diabetes insipidus: rapid postoperative correction. 188 51

Lithium may induce all clinical physiological abnormalities of the polydipsia- polyuria syndrome. Authors describe a 61-year-old woman patient in whom permanent disturbance of the water metabolism, nephrogenic diabetes insipidus (NDI) was caused by lithium treatment, lasting longer than 10 years. The partial resistance of the fluid disturbance to vasopressin has been investigated by the administration of supramaximal doses of dDAVP. Considering the known antidiuretic effect of indomethacin, authors compared antidiuruetic activity of indomethacin and piroxicam (Hotemin) by studying standard parameters of water metabolism/free water clearance ect.) It was found that piroxicam, on mg basis a more effective antiinflammatory compound, was less antidiuretic then indomethacin. It was concluded, that there is no close parallelism between the structure and antiinflammatory and antidiuretic activity of nonsteroid antiinflammatory drugs. In the opinion of authors nonsteroid antiinflammatory drugs may have a role in the treatment of lithium-induced NDI, though, the establishment of the safety use of such therapy requires further studies.
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PMID:[Lithium-induced chronic water-metabolism disorder (nephrogenic diabetes insipidus)]. 192 71

A total of 29 patients with severe hemorrhagic fever associated with the renal syndrome were studied for impact of extracorporeal hemodialysis on the activity of the renin-aldosterone system (RAS), plasma vasopressin and osmolality and the levels of the major osmotically active agents, as well as the circadian urine output and blood pressures. In patients with oliguria there was a significant activation of RAS, an increase in plasma vasopressin ad osmolality due to the increment of the urea in presence of hyponatremia. Hemodialysis led to a temporary normalization of plasma aldosterone and vasopressin levels and a decrease in blood pressure. No significant changes were documented in the activity of the plasma renin and circadian urinary output. A direct correlation was established between the plasma osmolality and the levels of vasopressin. In patients with polyuria developed in presence of hypernatremic hyperosmia plasma vasopressin elevated and aldosterone dropped.
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PMID:[The effect of hemodialysis on the vasopressin level and on the renin-aldosterone system in patients with hemorrhagic fever with renal syndrome]. 197 Sep 14

In a brief review the author presents selected results of endocrinological research, published in 1989 to 1990. In the sphere of peptide hormones he mentions findings on the reduced level of the endothelial relaxation factor in the blood stream in atherosclerosis, the classification of endothelin with neuropeptides and the existence of a vasopressin antagonist which causes polyuria after operations of the hypothalamus. Hybrid hormones (biotechnologically prepared combined molecules), mammastatins (inhibitors of proliferation of mammary cell cultures lacking in transformed cultures) and adipsin (a peptide factor lacking in some types of experimental obesity) are other recent advances. Findings on endogenous benzodiazepine substances (occupying receptors for diazepines) and of an endogeneous factor for receptors for tetrahydrocanabinols supplement the contemporary picture. Adrenocortex stimulating immunoglobulins may be the cause of hyperplasia of the adrenal cortex, similarly as TSI is the cause of Graves-Basedow's disease. In the latter evidence of a retroviral aetiology was provided.
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PMID:[Endocrinology 1989-1990]. 207 Mar 86

The urinary concentrations of prostaglandins(PG) E2, 6-keto-PGF1 alpha (6KPGF) and thromboxane (Tx) B2 were measured by RIA method during both hypotonic polyuria (oral water load) and subsequent antidiuresis (low-dose infusion of lysine-8-vasopressin). The study was performed on healthy women either in normal potassium balance (N, n = 14) or sustained potassium depletion (D3, n = 6). Potassium depletion (KD) was induced by low potassium dietary intake (less than or equal to 10 mmol/d) and natriuretic treatment over a period of 8 days; the net losses of NaCl and H2O were replaced; the cumulative potassium deficit was 198 +/- 22 mmol. Further studies were performed after indomethacin treatment in both experimental conditions. 1) As compared to normal potassium balance in KD group the urinary prostanoid excretions were reduced even in absence of significant differences in urinary flow rate. The urinary excretion of 6KPGF was more impaired than that of TxB2 in both polyuria and antidiuresis. 2) Indomethacin inhibited the urinary prostanoid excretions in normal potassium balance and KD groups. The urinary excretion of PGE2 was more impaired than that of both 6KPGF and TxB2.
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PMID:[Selective inhibitory effects of experimental potassium depletion on urinary excretion of prostanoids and their possible functional significance]. 207 86


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