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)

The effects of vasopressin administered by continuous infusion (0.75 and 0.5 mU/m2/minutes) was studied in two groups of three normal and two groups of 5 and 8 malnourished children given 0.5 and 0.3 mU/m2/minute. The following parameters were analyzed: urine volume, osmolality, water reabsorption, PAH, urea and inulin clearances, Na and K urinary excretion. Malnourished children had a urine volume 3 to 5 times higher than the normal groups. Vasopressin increased urine volume initially, but a mild antidiuretic effect followed in the normal groups. In malnourished children with a high CH2O, antidiuresis showed quite important figures with vasopressin. A transient fall in PAH and inulin clearances was observed with vasopressin in both malnourished groups with a mild drop in the normal group. Natriuresis with a higher % of the filtered sodium excretion was observed in the malnourished groups and in normal children with 0.5 mU of vasopressin. These results show that vasopressin had similar effects, but at a different level in the normal and malnourished children that we studied.
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PMID:[Renal function in normal and malnourished children given different doses of vasopressin in continuous infusion]. 46 71

Renal function was examined in twelve patients, eight girls and four boys, with anorexia nervosa (AN) ranging in age from 12.6 to 18.2 years. The weight loss at the time of the study averaged 26%. Determinations were made of glomerular filtration rate (GFR), PAH clearance (CPAH) and urinary concentrating capacity. For references the same studies were also carried out in five healthy teenagers. Both GFR and CPAH were generally CPAH as shown by a significantly lower filtration fraction (FF) in AN. Indirect evidence suggests that the low FF could be attributed to reduced water permeability of the glomerular capillary. The urinary concentrating capacity following fluid deprivation was moderately depressed both before and after the administration of vasopressin. The concentrating defect in AN must therefore be primary of renal origin.
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PMID:Renal function in anorexia nervosa. 62 79

Renal effects of large doses of fentanyl (1 mg/kg) were determined in 14 mongrel dogs before and after addition of 50 per cent nitrous oxide. Fentanyl significantly increased urine osmolarity and decreased urine output and free water clearance but did not change inulin or PAH clearances. The arterial blood pressure and cardiac output were significantly decreased after 0.1 mg/kg fentanyl and these changes were then maintained during the remainder of the study period. Addition of nitrous oxide produced no further changes in cardiac output and arterial blood pressure but did increase urine output, PAH, inulin and free water clearances and decreased urine osmolarity. These data demonstrate that high doses of fentanyl have significant antidiuretic properties in the dog and these probably are related to the release of antidiuretic hormone. Our results also indicate that addition of nitrous oxide reverses fentanyl induced antidiuresis.
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PMID:The effects of large doses of fentanyl and fentanyl with nitrous oxide on renal function in the dog. 93 67

Renal clearances and plasma antidiuretic hormone (ADH), 17-hydroxycorticoids, and norepinephrine were measured in unrestrained dogs before and during exposure to ambient cold (minus 4 to + 4 degrees C). Some dogs were treated with an inhibitor of cortisol biosynthesis, Metopirone, either alone or combined with dexamethasone, a potent glucocorticoid suppressing ACTH release. Plasma ADH increased in the Metopirone-treated group (P smaller than 0.02) but changed little in other dogs. Plasma 17-hydroxycorticoids in untreated dogs rose from a control value of 14.4 plus or minus 1.9 (SE) to 1.82 plus or minus 1.2 mug/100 ml after 20 min of exposure (P smaller than 0.01), an increase comparable with that previously observed in restrained dogs. Plasma norepinephrine increased from 0.98 plus or minus 0.07 to 1.15 plus or minus 0.08 mug/liter (P smaller than 0.01) after 20 min of exposure. Urine flow, C-Cr, and C-PAH tended to increase spontaneously in nonexposed control dogs. Exposure to cold abolished or reversed this tendency, most distinctly in the Metopirone-dexamethasone group. The urine concentration, measured as T-c-H2O/C-Cr, did not change in cold, in contrast to a decrease previously observed in restrained dogs. The data do not support the key role of plasma cortisol elevation in the mechanism of urine-concentration defect in cold and demonstrate important differences between responses of restrained and unrestrained animals.
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PMID:Plasma hormone and renal function changes in unrestrained dogs exposed to cold. 111 60

We describe our observations concerning differences in two groups of young hypertensive patients according to their renin activities after ACE inhibition. Seventeen of these patients (age 26 +/- 7 years), so far untreated, were investigated prospectively for hormone levels (renin, aldosterone, vasopressin), microalbuminuria, renal haemodynamics (inulin and PAH clearance) and signs of organ damage (echocardiography, fundoscopy). Secondary forms of hypertension were excluded by routine methods, including angiography. We differentiated two groups of young hypertensive patients. Group 1 (n = 9) had a false positive captopril test with elevated renin activities after ACE inhibition with captopril (8.4 +/- 5 ng/ml per hour) compared to group 2 (renin activity: 2.2 +/- 1.3 ng/ml per hour) or an increase of greater than 400% of renin activity after ACE inhibition. Baseline renin activities and sodium excretion did not differ between the groups. Group 1 also showed significantly greater GFR, FF, and microalbuminuria, as well as signs of organ damage, with left ventricular hypertrophy and hypertensive changes in fundoscopy. There were no differences between the groups concerning mean arterial blood pressure and duration of hypertension. In conclusion, we were able to demonstrate that patients with highly stimulated renin activities showed signs of visceral organ damage and renal hyperfiltration compared to the normal renin activity group after ACE inhibition. Investigations of the renin-angiotensin-aldosterone system with ACE inhibitors might constitute a helpful indicator of renal changes and organ damages in young hypertensive patients.
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PMID:Renal haemodynamics and organ damage in young hypertensive patients with different plasma renin activities after ACE inhibition. 131 92

A role for arginine vasopressin has been implicated in the compensatory control of arterial blood pressure in several animal models with reported increases in plasma levels of arginine vasopressin. A threefold elevation in plasma vasopressin has been reported in conscious dogs following constriction of the inferior vena cava. In the present study, infusion of the arginine vasopressin antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-O-methyltyrosine] Arg8-vasopressin into conscious dogs with chronic caval constriction did not decrease mean arterial blood pressure. However, the dose of infused antagonist completely blocked the pressor response to 2 micrograms of exogenous vasopressin. Also the antagonist produced no effect on heart rate, plasma renin activity, or urinary volume and electrolyte excretions. A slight, transient increase (P less than or equal to 0.05) was observed in creatinine clearance and in PAH clearance following antagonist infusion, suggesting a possible decrease in renal vascular resistance. These data suggest that the direct vasoconstrictor actions of vasopressin contribute minimally, if at all, to blood pressure maintenance following chronic caval constriction. Alternatively, blockade of endogenous vasopressin receptors at the level of peripheral arterioles may have resulted in no depressor response due to a masking of this response by other compensatory hormonal and neural pressor systems.
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PMID:Systemic and renal hemodynamic responses to vascular blockade of vasopressin in conscious dogs with ascites. 298 53

Nitrofen and ethylenethiourea (ETU), agents known to prenatally induce hydronephrosis in rats, were assessed for their effects on postnatal renal functional maturation. Both were given by gavage to pregnant Sprague-Dawley rats on Gestation Day 11. Nitrofen was given at concentrations of 50 or 100 mg/kg, and ETU at 20, 40, or 60 mg/kg. Renal function was examined in the offspring from birth until after weaning, the period of renal functional maturation in the rat. Maximal urine concentrating ability was measured after DDAVP (desmopressin acetate, a vasopressin analog) challenge or water deprivation. Proximal tubule transport was measured in renal cortical slices. Various urinary parameters were measured. Both prenatal nitrofen and ETU exposure caused a large number of neonatal deaths at the high dose, and hydronephrosis was observed. The severity of the lesion increased with age. Hydronephrotic animals were deficient in urine concentrating ability, which became more pronounced after weaning. A few other urinary parameters were altered, but cortical function appeared to be unaffected. Rats prenatally exposed to nitrofen, but with apparently normal kidneys, were significantly compromised in their ability to produce a concentrated urine in response to DDAVP challenge, on Postnatal Days (PDs) 6 and 14. By PD 30, they were not different from controls in urine concentrating response. Rats prenatally exposed to the higher doses of ETU, but with grossly normal kidneys, had significantly decreased plasma clearances of certain electrolytes early in life, but by PD 27, they were not different from controls. Proximal tubule transport of PAH was increased on PD 7 in ETU-exposed pups, but this effect did not persist.
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PMID:Functional teratogens of the rat kidney. II. Nitrofen and ethylenethiourea. 322 Feb 15

Decreased urinary output (Vu ml/min) after institution of PEEP is attributed to a variety of mechanisms including decreased cardiac output and renal blood flow (RBF), activation of neurohormonal reflexes, increased catecholamines, plasma renin activity (PRA), and antidiuretic hormone (ADH) release. To evaluate these factors, seven normovolemic patients (36 yr +/- 13 SD), free of preexisting lung, cardiac, or renal disease, requiring continuous mandatory ventilation for neurologic reasons were studied. The authors measured or calculated: total blood volume (TBV) (51Cr); right atrial, pulmonary arterial, pulmonary wedge, and systemic pressures, cardiac index (CI); renal plasma flow (RPF) (iodohippurate sodium 131I [131I PAH] clearance); glomerular filtration rate (GFR) (creatinine clearance), free water clearance (CH2O), osmolal clearance (Cosm), fractional excretion of sodium (FENa+) and potassium (FEK+); and plasma renin activity (PRA) (ng X ml-1 X h-1), plasma ADH (pg/ml; radioimmunoassay), epinephrine (E in pg/ml), and norepinephrine (NE in pg/ml) (double-isotope radioenzymatic assay). Two conditions were studied after 90-min steady state: 1) zero PEEP (ZEEP); and 2) 15 cmH2O PEEP. PEEP caused a significant decrease in CI (-21%; P less than 0.01) and RPF (-19%; P less than 0.05) without significant decrease in GFR. A significant decrease in Vu (-55%; P less than 0.05), FENa+ (-39%; P less than 0.05) and Cosm (-36%; P less than 0.25) occurred without modification in CH2O. Plasma ADH remained in the normal range and did not increase when PEEP was applied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:No involvement of antidiuretic hormone in acute antidiuresis during PEEP ventilation in humans. 354 90

The increased renal sodium and water excretion after an intravenous infusion of Ringer solution has been investigated in anaesthetized dogs. The response of the kidneys has been examined in four combinations. The functional parameters of renal function have been compared during volume expansion by 1.5-2.0% body weight Ringer solution and overhydration by 2.5% Ringer solution for 60 min. In the control animals, volume expansion by 2% body weight Ringer solution resulted in a significant increase in sodium excretion and urine flow. When these animals were infused with 2.5% body weight Ringer solution a marked increase in water excretion was observed with a smaller increment in sodium excretion, and the urine became hypo-osmotic as compared to the plasma. No difference was found in glomerular filtration rate and PAH clearance. In the group No. 2, the effect of 4 mg/kg indomethacin infusion was studied. The inhibition of prostaglandin synthesis considerably reduced the diuretic effect of Ringer infusion and did not affect sodium excretion. In the group No. 3, the animals received lysine-8-vasopressin i.v. in a preliminary dose of 10 mU/kg during 10 min and then 50 mU/kg over 60 min in infusion. Volume expansion with 2.5% body weight of Ringer solution resulted in a marked increase in sodium and water excretion but no difference was found in glomerular filtration rate and PAH clearance. Dilution of the urine i.e. a decrease of urinary osmolarity, in spite of the vasopressin infusion, was significantly higher in this group than in the control animals (group No. 1). In the fourth series, after 4 mg/kg of indomethacin the same dose of vasopressin was administered as in group No. 3. Indomethacin was observed to inhibit the diuretic effect of vasopressin and did not affect the saluretic effect. From these data it was concluded that medullary tonicity affected renal water handling during extracellular isosmotic hypervolaemia induced by Ringer infusion. This mechanism depends on medullary prostaglandin synthesis and is independent from the plasma vasopressin concentration. Our findings clearly indicate that extracellular hypervolaemia increases renal sodium excretion and lysine-8-vasopressin was found to potentiate this effect. This sodium excretion increasing mechanism does not depend on renal prostaglandin secretion, nor were glomerular factors responsible for the increase of sodium and water excretion.
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PMID:Inhibition of prostaglandin synthesis and the action of vasopressin during extracellular volume expansion in the dog. 665 Jan 87

Infusion of noradrenaline at rates between 32-160 nmol.min-1 for 30 min into one lateral cerebral ventricle of conscious sheep caused a diuresis which was accompanied by negative solute-free water reabsorption and which lasted for 90-120 min. The range of noradrenaline infusion rates used reflects differences between individual animals in the rate of infusion necessry to cause diuresis. Intracerebroventricular (ICV) infusion of noradrenaline at half the diuretic rate caused no significant changes in urine flow. The diuresis induced by ICV noradrenaline infusion was prevented by concurrent ICV administration of the alpha-adrenergic antagonist, phentolamine, but was not prevented by concurrent ICV administration of the beta antagonist, propranolol, or by concurrent intravenous infusion of phentolamine. Intravenous infusion of noradrenaline at rates that were diuretic by ICV infusion caused a diuresis of approximately 30 min duration which coincided with the period of intravenous noradrenaline infusion. This diuresis was prevented by concurrent intravenous infusion of phentolamine. These results were interpreted as indicating that the higher rates of ICV infusion of noradrenaline caused the prolonged water diuresis by acting at a site in the brain and, thereby, inhibiting the release of endogenous vasopressin. ICV infusion of noradrenaline at all rates was followed by a reduction in mean arterial blood pressure and pulse pressure with variable changes in heart rate and by depression of the rates of renal clearance of PAH, potassium and total solute.
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PMID:Diuretic effect of intraventricular and intravenous infusions of noradrenaline in conscious sheep. 690 39


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