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 experiments were performed on male rats, drinking 2% NaCl solution ad libitum for 12 days instead of tap water. The pituitary gland was exposed by the transpharyngeal approach under urethane-chloralose anaesthesia. The posterior lobe remained in neural and partial vascular connection with the hypothalamus, whereas the anterior lobe was entirely removed. Samples of the outflow medium from the incubated in situ rat posterior pituitary lobe were collected during 30 min intervals. Substance P-like peptides and vasopressin activities were assayed by the biological tests. Injections of hypertonic solution into the internal carotid artery did not change vasopressin release, but induced an increase in Substance P release from the posterior pituitary lobe into the incubation medium. Under conditions of unexcitability of the osmosensitive cells, triggering vasopressin release, the injection of hypertonic solution into the internal carotid artery stimulated the Substance P-like peptides release from the posterior pituitary lobe.
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PMID:Substance P-like peptides and vasopressin release from posterior pituitary lobe incubated in situ after intracarotid injections of hypertonic solution in rats. 2 85

Rats given ethanol in their drinking water at a concentration that permitted adequate fluid intake gradually accepted higher concentrations and consumed larger amounts of ethanol. These increases were augmented when daily subcutaneous injections of 1 microgram of desglycinamide9-lysine8-vasopressin (DGLVP) or 10 microgram of prolyl-leucyl-glycinamide (PLG) were given concomitantly. Nonsignificant changes in ethanol consumption were seen with injections of 1 microgram PLG, or 0.42 or 42 microgram of lysine8-vasopressin (LVP). In a second experiment 4 microgram DGLVP given every second day as a long-acting zinc phosphate complex, commencing after the increases in ethanol intake had taken place, failed to produce any change in ethanol consumption subsequently. In both Experiments 1 and 2, the rats were switched from forced ethanol intake to a choice between ethanol and tap water. On these tests there was only marginal evidence of peptide-produced changes in ethanol intake.
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PMID:Effect of desglycinamide(9)-lysine(8)-vasopressin and prolyl-leucyl-glycinamide on oral ethanol intake in the rat. 3 34

In previous studies we found that vasopressin stimulation of both cyclic AMP (cAMP) formation in cortical collecting tubules (CCT) and sodium reabsorption in isolated perfused kidneys was markedly exaggerated in rats with mineralocorticoid hypertension. In the present study, we tested the response (cAMP accumulation) of cortical and outer medullary collecting tubules (OMCT) to vasopressin in two rat models that are resistant to deoxycorticosterone acetate (DOCA)-induced hypertension, the Wistar-Furth strain and NaCl-deficient rats. The blood pressure of normal outbred Wistar rats rose to hypertensive levels (systolic pressure more than 165 mm Hg) during a 5-week treatment with DOCA (10 mg/week) and 1% saline to drink. Significant hypertrophy of the heart and kidneys was also observed. Vasopressin (10(-8) M)-induced cAMP formation was enhanced 3.4-fold in the CCT (OMCT unchanged) of hypertensive rats compared with normotensive controls. Significant hypertrophy (as indexed by tubule diameter) of the CCT but not the OMCT was also observed in DOCA-salt hypertensive rats. Restriction of dietary NaCl (0.13% in chow, tap water to drink) completely prevented DOCA-induced hypertension, organ and CCT hypertrophy, and enhancement of vasopressin-stimulated cAMP formation in the CCT. In Wistar-Furth rats, DOCA-salt treatment did not alter blood pressure or cause significant organ hypertrophy. However, DOCA-salt treatment enhanced vasopressin-stimulated cAMP formation by 4.1-fold in CCT of Wistar-Furth rats, with significant tubular hypertrophy in the CCT but not the OMCT. We conclude that DOCA-induced hypertension and changes in CCT function are dependent on excess dietary NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin response in collecting ducts of rats resistant to mineralocorticoid hypertension. 184 20

Male Sprague-Dawley rats were uninephrectomized and given either deoxycorticosterone (DOC) pivalate (12.5 mg three times weekly) and 1% NaCl/0.2% KCl to drink for 4 weeks (DOC-treated), after which DOC was stopped and tap water substituted (post-DOC), or tap water to drink throughout (controls), DOC treatment increased blood pressure, serum sodium, plasma atrial natriuretic peptide (P-ANP) and plasma deoxycorticosterone (P-DOC) (P less than 0.05), while serum potassium, plasma renin and plasma angiotensin II were lower (P less than 0.05) than in control animals. Plasma vasopressin (P-AVP) was also raised but not significantly. These changes persisted for up to 4 weeks post-DOC and, in the case of plasma renin, plasma angiotensin II, P-AVP and P-ANP, for up to 12 weeks. Total body sodium was also increased at 2 weeks post-DOC (P less than 0.05). Rats which were adrenalectomized after 4 weeks of DOC treatment in which DOC injections were stopped, then drank either NaCl/KCl or tap water; blood pressure and P-DOC remained elevated while plasma renin remained suppressed. There were more deaths in rats given NaCl/KCl (five of six) than in the group given water (one of six). Rats treated with a subcutaneous DOC silastic implant had a comparable rise in blood pressure to rats given DOC injections. However, after removal of the implant, while blood pressure remained elevated, P-DOC levels were not raised and plasma renin rose to control levels after 4 weeks. These findings indicate that, in rats given DOC injections, post-DOC hypertension results from sodium and fluid retention as a consequence of chronic hangover of exogenously administered DOC.
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PMID:Hormone and electrolyte changes in post-deoxycorticosterone salt hypertension in rats. 196 84

A messenger ribonucleic acid (mRNA) homologous to the transcript that encodes vasopressin (VP) was detected in the neurointermediate lobe (NIL) of the rat pituitary. The abundance of this transcript is approximately 1/100th the amount detected in the hypothalamus. In rats drinking 2% NaCl-water for 0,2,4, or 10 days, or for 10 days and then tap water for 14 days, the levels of VP mRNA in the NIL were altered in a fashion that paralleled changes in the hypothalamus.
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PMID:Detection of vasopressin mRNA in the neurointermediate lobe of the rat pituitary. 217 10

1. The measurement of cellular mRNA content by quantitative in situ hybridization is a valuable approach to the study of gene expression in brain since this tissue exhibits a high degree of phenotypic heterogeneity. 2. The cellular content of vasopressin and oxytocin mRNA in hypothalamo-neurohypophysial system neurons was altered by maintaining rats for 24 hr on 2% sodium chloride water. 3. Statistical and graphical techniques were then used to analyze cell by cell how mRNA levels were altered as a result of osmotic stimulation. We propose that the negative binomial probability distribution is a suitable model to describe how mRNA content varies across a defined cell population. For both measures of oxytocin and vasopressin mRNA levels, maximum-likelihood estimation indicated that this model adequately described empirical findings obtained from rats drinking tap water or salt water. 4. Both graphical and statistical analyses suggested how the defined neural system responds to osmotic stimulation: mRNA content was altered as a multiplicative function of "initial state." The utility and limitations of the quantitative approach are discussed.
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PMID:Quantitative in situ hybridization to measure single-cell changes in vasopressin and oxytocin mRNA levels after osmotic stimulation. 233 46

The deoxycorticosterone acetate (DOCA)-Na model of hypertension requires the presence of vasopressin for expression of high blood pressure. In the present study, the effects of vasopressin V2-receptor stimulation were examined in kidneys from rats receiving 1 wk of DOCA-Na or control (olive oil-tap water) treatment. The dose response to vasopressin (10(-10) to 10(-6) M) was tested in microdissected cortical collecting tubule (CCT) segments and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation was significantly increased in segments from DOCA-Na rats vs. controls, confirming our previous study. In other experiments, kidneys from DOCA-Na and control rats were perfused with a modified Krebs-Henseleit buffer (37 degrees C, pH 7.4) and treated with either vehicle or 0.21-2.1 pM 1-desamino-8-D-arginine vasopressin (DDAVP). DDAVP caused significant (P less than 0.05) dose-related reductions in urine excretion (UV) and urinary sodium excretion (UNaV) in both DOCA-Na and control kidneys in the absence of changes in renal hemodynamics. However, DDAVP produced earlier and significantly greater reductions in UV and UNaV in kidneys from DOCA-Na vs. control rats. Percent fractional excretion of sodium was reduced significantly only in the DOCA-Na group (2.1 pM DDAVP). A small degree of antikaluresis was seen with DDAVP in both groups. Thus, DOCA-Na treatment augmented cAMP accumulation in the CCT, accompanied by a significant enhancement of DDAVP-stimulated urinary sodium and water reabsorption at the level of the intact kidney.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced vasopressin (V2-receptor)-induced sodium retention in mineralocorticoid hypertension. 283 67

The role of atrial natriuretic peptide (ANP) in the extracellular volume expansion (ECVE) induced natriuresis was examined in normal man under basal conditions and following dopamine blockage. Hypotonic ECVE was induced by drinking of 20 ml/kg tap water and subsequent intravenous infusion of 2 1 0, 9% saline over a period of 4 hours. This maneuver caused an increase in the plasma concentrations of ANP from 25.8 +/- 3.4 (means +/- SEM) to 59.7 +/- 6.7 fmol/ml. There was a dissociation between ANP response and urinary sodium excretion. A transient rise in glomerular filtration rate (GFR), plasma dopamine and a continuous decrease in plasma renin activity, aldosterone, vasopressin, and noradrenaline were observed. The natriuretic response to ECVE was blunted during dopamine blockade by metoclopramide, but plasma ANP, renin activity, catecholamine and vasopressin levels were not affected. However, plasma aldosterone rose. Our data are compatible with the concept that intrarenal dopamine and raised plasma concentration of ANP contribute to the natriuretic response to ECVE, but these hormonal changes do not completely explain the underlying mechanisms.
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PMID:Atrial natriuretic peptide in volume expansion-induced natriuresis in man. 296 21

This study investigated the effects of treatment with desoxycorticosterone acetate and salt (DOCA/NaCl) on blood pressure, aortic vascular vasopressin receptors and in vitro vascular responsiveness in male rats. Four groups of animals were utilized in the study: a control group on normal tap water, a control group drinking a 1% NaCl solution; a DOCA/NaCl-treated group (1% NaCl in the drinking water); and a uninephrectomized (1K) DOCA/NaCl-treated group. DOCA/NaCl treatment for 4 weeks resulted in a significant elevation in blood pressure which was more pronounced in the uninephrectomized animal. The concentration of specific binding sites for vasopressin on the aorta were reduced in both the DOCA/NaCl-treated groups. However, the vascular responsiveness of the aorta to vasopressin was significantly reduced only in the hypertensive, uninephrectomized-DOCA/NaCl-(1K DOCA/NaCl) treated rat. Both the maximal contraction and the sensitivity was reduced in the 1K DOCA/NaCl group. The results of this study would suggest that the vascular alterations to vasopressin are probably post receptor mediated and result from the DOCA/NaCl-induced hypertension.
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PMID:Changes in vascular vasopressin receptors and responsiveness in DOCA/NaCl-treated rats. 296 70

To investigate whether paracentesis could be an alternative therapy for ascites, 117 cirrhotics with tense ascites were randomly allocated into two groups. Fifty-eight patients (group 1) were treated with paracentesis (4-6 L/day until disappearance of ascites) and intravenous albumin infusion (40 g after each tap). Fifty-nine patients (group 2) were treated with spironolactone (200-400 mg/day) plus furosemide (40-240 mg/day). Patients from group 2 not responding to diuretics were treated with a LeVeen shunt. After disappearance of ascites, patients from both groups were discharged from hospital and were instructed to take diuretics. Patients developing tense ascites during follow-up were readmitted to hospital and treated according to their initial schedule. Paracentesis was effective in eliminating the ascites in 56 patients from group 1 (96.5%) and did not induce significant changes in renal and hepatic function, plasma volume, cardiac index, peripheral resistance, plasma renin activity, plasma norepinephrine and antidiuretic hormone concentration, and urinary excretion of prostaglandin E2 and 6-keto-prostaglandin F1 alpha. Diuretics were effective in eliminating the ascites in 43 patients from group 2 (72.8%) (p less than 0.05). Ten patients in group 1 and 36 in group 2 developed complications during their first hospital stay (p less than 0.001). This difference was due to the significantly higher incidence of hepatic encephalopathy, renal impairment, and electrolyte disturbances occurring in patients treated with diuretics. The duration of hospital stay was 11.7 +/- 1.5 days for patients from group 1 and 31 +/- 2.8 days for patients from group 2 (p less than 0.001). The two groups did not differ significantly with respect to the probability of requiring readmission to hospital during follow-up, reasons for readmission, survival probability after entry into the study, and causes of death. These results indicate that paracentesis associated with intravenous albumin infusion is a fast, effective, and safe therapy for ascites in patients with cirrhosis.
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PMID:Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Results of a randomized study. 329 7


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