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)

In unanesthetized water-loaded rats, intracerebroventricular (IVT) angiotensin II (AII) injections produce centrally mediated pressor effects and antidiuresis. Experiments were performed to evaluate the role of antidiuretic hormone (ADH) release versus neurogenic mechanisms in the antidiuretic responses to central AII median eminence lesions used to block ADH release abolish antidiuretic effects but only attenuated pressor responses to IVT AII infusions. Pretreatment with an intravenous infusion of ADH antibody had a similar effect. Central administration of AII in water and saline-loaded rats produced no change in effective renal plasma flow or glomerular filtration rate, Natriuretic and kaliuretic responses to IVT AII injections were similar to those observed to intravenous ADH infusions. These data are consistent with the suggestion that antidiuresis and osmotic excretion observed after IVT AII injections in the rats are the result of ADH release, and that neurogenic mechanisms play a major role in the blood pressure but not in the antidiuretic responses.
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PMID:Central effects of angiotensin II in water and saline loaded rats. 44 May 32

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

A simple efficient procedure for extracting and concentrating arginine-8-vasopressin (AVP) from urine has been coupled with a specific and sensitive radioimmunoassay in order to measure antidiuretic hormone (ADH) excretion in normal humans under various physiological stimuli. Antisera have been raised in rabbits injected with lysine-vasopressin (LVP) or AVP coupled with bovine serum albumin. The antiserum selected for the assay which inhibits the antidiuresis induced in the rat by AVP is used at a final dilution of 1 : 50,000 and possesses a high association constant of 1 x 10(11) 1.mol-1. The limit of detection of the RIA system is 0.5 micronUI/ml of urine (1.25 pg). Urinary ADH has been extracted from urine by Miller and Moses method. Mean recovery of added vasopressin averaged 90.2% +/- 11 (SD) and assay of serial dilutions of such extracts showed that they behave in the assay system in the same way as synthetic AVP standards. Moreover comparison of the results obtained by the RIA to those given by the biological method using the ethanol anesthetized rat showed excellent correlation (r = 0.9 p less than 0.001). Under ad libitum fluid and food intake, mean daily urinary excretion of AVP (uncorrected for recovery) determined in 22 subjects was found to be 30.58 +/- 11.64 mU/h with no significant difference between men and women. In response to an oral waterload ADH became undetectable at the peak of diuresis. Following a 16 hr fluid deprivation, ADH rose moderately. A significant correlation has been found between urine osmolality and AVP excretion rate.
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PMID:[Radioimmunoassay of ADH in human urine (author's transl)]. 47 16

Hyponatremia with simultaneous renal sodium loss was associated with the inappropriate secretion of antidiuretic hormone in a dog with heartworm disease. Antidiuresis caused expansion of extracellular fluid volume, which induced renal salt wasting and a negative sodium balance. The combination of water retention, salt wasting, and inactivation of intracellular solute contributes to the decrease in serum sodium concentration. Water intoxication due to hypotonicity of body gluids induced anorexia, depression, weakness, and incoordination.
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PMID:Inappropriate secretion of antidiuretic hormone in a dog. 50 Apr 39

1. The effect of restricted water intake followed by voluntary rehydration with water or 10 mM-KCl was studied in four conscious sheep with respect to plasma concentrations of renin, antidiuretic hormone (ADH), protein and electrolytes, and urine flow rate, osmolality and osmolal excretion. 2. Water restriction increased the plasma renin concentration and the plasma ADH concentration. 3. Rehydration with water caused a further rise in plasma renin, but plasma ADH returned to basal levels in less than 2 hr. 4. Rehydration with 10 mM-KCl in order to stabilize plasma K concentration greatly attenuated the post-drinking rise in plasma renin concentration, while plasma ADH levels fell as before. 5. Urine flow rates after rehydration with water and 10 mM-KCl remained low for at least 6 hr in most experiments despite low plasma ADH levels. The effect on urine osmolality ranged from no change to a large drop. 6. The post-drinking antidiuresis was associated with a reduction in solute excretion rate. However, free water clearance usually remained negative. 7. These experiments do not support the existence of a direct nexus between plasma ADH levels and plasma renin concentration.
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PMID:Renin, antidiuretic hormone and the kidney in water restriction and rehydration. 51 41

Intravenous injection of 20 International Units (IU) of oxytocin in the form of synthetic oxytocin or neurohypophyseal extract preparations to dehydrated cows that had already undergone twelve hours of water withdrawal did not produce antidiuresis but rather rise of diuresis accompanied by saluretic effects. Increase in diuresis occurred also in hyperhydrated cows, following water application, provided that oxytocin or vasopressin preparations had caused antidiuresis and saluresis and, consequently, changed urine composition to osmotic pressures beyond the limit values between 650 and 750 mosmol/kg. Rehydration of cow may be associated with retardation of diuresis by four hours or more. If oxytocin or vasopressin are given in the phase of such rehydration, the period between water application and the onset of water diuresis may be defined as "blocked water diuresis". Continuous infusion of 0.34 or 0.8 IU of oxytocin per minute up to 3.5 hours did not cause water intoxication in hyperhydrated cows, though blood plasma values for osmotic pressure had dropped to 244 mosmol/kg, while Na+ concentration had gone down to 116 mmol/l.
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PMID:[Studies of the induction of diuresis increase and water intoxication induced diuresis inhibition by oxytocin and vasopressin in lactating cattle]. 54 13

Thermoregulatory reactions evoked by selective preoptic-anterior hypothalamic (PO/AH) heating in conscious rabbits were associated with significant changes in renal function. Urine flow rate decreased from a control value of 0.92 +/- (S.E.) 0.08 to 0.47 +/- 0.07 ml/min after 10-20 min of heating, urine osmolality increased from 273 +/- 34 to 417 +/- 46 Osm/kg H2O, and free water clearance per 100 ml GFR decreased from 1.11 +/- 0.46 to -0.50 +/- 0.23 ml/min. These changes were followed by a gradual recovery despite continued heating. Clearances of exogenous creatinine and p-aminohippurate fell transiently during the first 10 min of heating and then returned to normal. Plasma antidiuretic activity (ADA) measured by rat bioassay increased regularly and markedly during PO/AH heating but was poorly correlated with changes in urine concentration. Moreover, a similar increase in plasma ADA observed with selective heating of a different brain area (supraoptic nucleus) never produced urine concentration or other renal changes. This suggests that a large and variable fraction of ADA appearing in rabbit blood in response to thermal stimuli was not identical with antidiuretic hormone. Therefore, the causal relationship of ADH release and antidiuresis associated with thermoregulatory reactions could not be clearly demonstrated. The physiological role of renal water conservation would be to compensate for extrarenal water loss related to thermal sweating or panting.
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PMID:Renal function changes during preoptic-anterior hypothalamic heating in the rabbit. 56 82

Five antidiuretic drugs were administered in each of twenty patients with cranial diabetes insipidus (DI). A daily intranasal dose of 10 microgram DDAVP (Adiuretin) produced longer and stronger antidiuretic effects than the posterior pituitary snuff, containing 100 microgram AVP, and than 12.5 microgram synthetic LVP spray, but a shorter antidiuresis than 12.5 microgram vasopressin tannate in oil, administered intramuscularly, antidiuresis lasting 14, 6, 4 and 36 hs respectively. Chlorpropamide produced an inconstant and less potent antidiuresis. 10microgram DDAVP given per nostril twice a day cancelled completely and without side effects DI in five patients with bronchospastic reaction to-pituitary snuff; the same daily dose was sufficient for the safe treatment of two DI women along pregnancy and lactation periods. It is recommended to use DDAVP as elective drug for the treatment of cranial DI.
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PMID:Effects of DDAVP in cranial diabetes insipidus as compared to other antidiuretic drugs. 56 14

The purpose of the present study was to reexamine the effect of antidiuretic hormone (ADH) and indomethacin (IM) on intrarenal blood flow distribution by applying the microsphere technique to trained consciuous dogs. ADH and IM were given separately and jointly during maximal water diuresis. ADH in itself caused moderate antidiuresis and marked natriuresis. Although IM by itself had no significant effect on urinary osmotic concentration or solute excretion it greatly enhanced the antidiuretic effect of ADH and abolished its natriuretic effect. Intrarenal blood flow distribution remained unchanged when ADH and IM were given separately but it was shifted toward the inner cortex when the drugs were administered simultaneously. Furthermore, transition from spontaneous antidiuresis to maximal water diuresis did not alter intrarenal blood flow distribution. The results indicate that ADH induced antidiuresis is dissociated from changes in intracortical blood flow distribution. However, the possibility that IM enhancement of ADH mediated antidiuresis is at least in part mediated by intrarenal hemodynamic changes cannot be excluded.
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PMID:Effect of antidiuretic hormone and indomethacin on intrarenal microsphere distribution. 56 42

Diuretic features of 1,4-dimorpholino-7-phenylpyrido[3,4-d]pyridazine (DS-511) were studied in rats and mice. DS-511 was similar in diuretic effect to that of hydrochlorothiazide (HC) in both species, but was more water diuretic and less potassium-releasing than HC. After oral administration of DS-511 to rats the diuretic effect promptly appeared and lasted for 4 to 5 h. These patterns on onset and duration were similar to those of furosemide and acetazolamide (AZ). DS-511 was effective in experimentally induced acidotic and alkalotic rats. When DS-511 was used in combinations with other diuretics such as HC, AZ and triamterene at their maximum effective doses, urine volume and sodium excretion further increased, but potassium did not. Diuretic activity of DS-511 was not reduced by daily oral administration for 10 days to rats. In rats DS-511 reversed antidiuretic hormone (ADH)-induced antidiuresis. These findings suggest that DS-511 differs in mode and/or site of action from the known diuretics.
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PMID:1,4-Dimorpholino-7-phenylpyrido[3,4-d]pyridazine (SD-511) as a new type of diuretic agent. 58 97


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