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)

To determine whether the renal sympatho-inhibition and bradycardia in responses to acute increases in arterial pressure are altered in the diabetic state, the renal nerve discharge and heart rate were measured in streptozotocin (STZ) induced diabetic (DIA) rats. Integrated renal sympathetic nerve activity and heart rate were measured before and during an acute increase in blood pressure in anesthetized (Inactin 0.1 g/kg, i.p.) control (vehicle) and DIA rats (Sprague Dawley rats injected with STZ 65 mg/kg i.p.). Blood glucose levels were significantly elevated in the DIA group compared with the control group. Baroreflex changes in renal nerve activity and heart rate were not significantly different in the DIA rats compared with control rats at a time when the renal sympatho-inhibition in response to acute volume expansion was blunted in the diabetic rats. In addition, blocking the effect of elevated angiotensin II in diabetic rats with the converting enzyme inhibitor enalapril did not change the baroreflex function in DIA rats compared with control rats. However, administration of vasopressin failed to potentiate the baroreflex in diabetic rats as it did in normal control rats. This study demonstrates that (1) the baroreflex function is normal in STZ induced diabetic rats unlike the volume reflex during the early phase of the disease, (2) blockade of the AII system does not alter baroreflex function in diabetic rats and (3) vasopressin fails to potentiate the baroreflex in diabetic rats as it does in the euglycemic normal rats.
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PMID:Baroreflex function in streptozotocin (STZ) induced diabetic rats. 778 88

Transgenic mice overexpressing a transthyretin promoter-ANF structural fusion gene have a life-long reduction in arterial blood pressure compared to nontransgenic littermates. The present study was designed to test the hypothesis that the high plasma level of ANF in the transgenic mice inhibits the renin-angiotensin and/or vasopressin systems, thereby causing the hypotension. Mice were anaesthetized with Inactin and arterial pressure and heart rate were monitored before and during Saralasin infusion and vasopressin V1 receptor blockade. Effectiveness of the blockade was determined by injection of angiotensin and vasopressin before and during Saralasin and V1 receptor antagonist administration. Saralasin was associated with hypotension in both transgenic and nontransgenic mice. The decrease in blood pressure was proportionally greater in the transgenic animals. Vasopressin receptor blockade had little effect on blood pressure in either group. Heart rates were not different between the groups during any maneuver. We conclude that the chronic hypotensive effect of ANF overproduction does not involve the inhibition of either renin-angiotensin or vasopressin systems. The data, however, suggest that the renin-angiotensin system may be stimulated in the ANF-transgenic mice.
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PMID:Blood pressure regulation in ANF-transgenic mice: role of angiotensin and vasopressin. 799 80

The present study was undertaken to determine the involvement of the two established vasopressin receptor subtypes (V1 and V2) in arginine vasopressin (AVP)-induced natriuresis and also to determine whether changes in mean arterial pressure (MAP) and/or the renally active hormones atrial natriuretic peptide (ANP), angiotensin II (AII) and aldosterone are a prerequisite for the expression of AVP-induced natriuresis. In Sprague-Dawley rats which were anaesthetized with Inactin (5-ethyl-5-(1'-methylpropyl)-2-thiobarbiturate) and infused with 0.077 mol NaCl/l, infusion of 63 fmol AVP/min was found to be natriuretic whereas an approximately equipotent dose of the specific V2 agonist [deamino-cis1,D-Arg8]-vasopressin (dDAVP) did not induce natriuresis. The specific V1 antagonist [beta-mercapto-beta,beta-cyclopenta-methylene-propionyl1,O-Me- Tyr2,Arg8]-vasopressin when administered prior to infusion of 63 fmol AVP/min did not inhibit AVP-induced natriuresis. AVP-induced natriuresis was not accompanied by changes in MAP or in the plasma concentrations of the renally active hormones ANP, AII or aldosterone. These results suggest that neither the V1 nor the V2 receptors subtypes are involved in AVP-induced natriuresis. In addition, it was found that changes in MAP, plasma ANP, AII or aldosterone concentrations were not a prerequisite for AVP-induced natriuresis.
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PMID:Arginine vasopressin-induced natriuresis in the anaesthetized rat: involvement of V1 and V2 receptors. 845 93

We tested the hypothesis that hypertension in atrial natriuretic peptide (ANP) knockout mice is caused in part by disinhibition of angiotensin II-mediated vasopressin release. Inactin-anesthetized F(2) homozygous ANP gene-disrupted mice (-/-) and wild-type (+/+) littermates were surgically prepared for carotid arterial blood pressure measurement (ABP) and background intravenous injection of physiological saline or vasopressin V(1)-receptor antagonist (Manning compound, 10 ng/g body wt) and subsequent intracerebroventricular (left lateral ventricle) injection of saline (5 microl) or ANP (0.5 microg) or angiotensin II AT(1)-receptor antagonist losartan (10 microg). Only (-/-) showed significant decrease in ABP after intracerebroventricular ANP or losartan. Both showed significant hypotension after intravenous V(1) antagonist, but there was no difference between their responses. We conclude that 1) vasopressin contributes equally to ABP maintenance in ANP-disrupted mice and wild-type controls; 2) permanently elevated ABP in ANP knockouts is associated with increased central nervous angiotensin II AT(1)-receptor activation; 3) disinhibition of central nervous angiotensin II AT(1) receptors in ANP-deficient animals does not lead to a significant increase in the importance of vasopressin as a mechanism for blood pressure maintenance.
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PMID:Increased central AT(1)-receptor activation, not systemic vasopressin, sustains hypertension in ANP knockout mice. 1084 9


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