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)

dl-Propranolol (0.8-1.6 mg/kg - h for 1 h) produced a transient two- to three-fold increase in sodium excretion in nondiuretic rats infused with Pitressin and aldosterone and in water diuretic rats. Sodium excretion increased more in rats depleted of renin by chronic Doca and salt administration than in rats maintained on a low salt diet. An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Therefore the natriuresis was not mediated by antidiuretic hormone, aldosterone, or renin-angiotensin. d-Propranolol did not produce a natriuresis. Prior treatment with phenoxybenzamine did not prevent the natriuretic response but chlorisondamine pretreatment did. The natriuresis is produced by beta blockade and requires post ganglionic nerve function but is independent of alpha receptors. dl-Propranolol decreased heart rate and cardiac output but systemic pressure did not fall and renal blood flow increased. This suggests a dopamine-mediated renal vasodilation and natriuresis. Haloperidol and pimozide, both dopamine blocking agents with minimal beta blocking effects, prevented the natriuretic response. We conclude that propranolol may increase sodium excretion directly by blocking beta receptors in the distal nephron and indirectly by dopamine-mediated renal vasodilation.
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PMID:Propranolol induces acute natriuresis by beta blockade and dopaminergic stimulation. 1 Oct 39

The present study was conducted to measure norepinephrine release during sympathetic nerve stimulation and to evaluate vascular reactivity in the isolated perfused mesenteric vasculature of normotensive and Doca-salt hypertensive rats. Significantly greater vasoconstrictor responses to periarterial nerve stimulation, norepinephrine, and vasopressin, but not to barium chloride, were observed in the mesenteric vasculature of the hypertensive rats in comparison with the control normotensive group. Norepinephrine release, measured as total tritium overflow, during periarterial nerve stimulation at 4 Hz for 2 min, was identical in both normotensive and hypertensive animals. Phentolamine (5.3 micro M) significantly increased tritium overflow, but to the same extent in the normotensive and the hypertensive mesenteric vasculature, suggesting that the negative feedback presynaptic alpha-adrenoceptor mechanism, which has been proposed to modulate transmitter release, was unaltered in this form of hypertension. These results indicate that hyperresponsiveness of the mesenteric vasculature to periarterial nerve stimulation in the hypertensive rats is due to increased sensitivity of the vascular alpha-adrenoceptor and not facilitation of the transmitter release. The increased vascular reactivity to norepinephrine and vasopressin may be involved in the maintenance of Doca-salt hypertension.
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PMID:Sympathetic nerve function and vascular reactivity in Doca-salt hypertensive rats. 625 76

Arterial pressure, sodium excretion, urine output, and plasma atrial natriuretic peptide (ANP) concentrations were measured before, during, and after a 3-h i.v. infusion of arginine-vasopressin (vasopressin; 20 ng/kg/min) in conscious Doca-salt hypertensive rats. Arterial pressure was 166 +/- 8 mm Hg before the infusion of vasopressin; in comparison, pressure was only 130 +/- 4 mm Hg 5 h after stopping the infusion. The fall in pressure after withdrawal of an equipressor dose of phenylephrine in hypertensive animals was much less. In sham normotensive rats, pressure did not fall below control levels after stopping either the vasopressin or phenylephrine infusion. Sodium excretion rates were higher during infusions of vasopressin than during phenylephrine infusions. However, the elevations observed during vasopressin were similar in the hypertensive (25.3 +/- 4.9 mumol/kg/min) and normotensive (22.9 +/- 2.7 mumol/kg/min) groups. Urinary output increased to a greater extent in the hypertensive rats during the infusions of both vasopressin and phenylephrine, but the increases were similar for the 2 pressor agents. Plasma levels of ANP were elevated during the infusions of vasopressin in the normotensive rats, but not in hypertensive rats. The results indicate that the fall in pressure associated with cessation of a pressor dose of vasopressin appears specific to the hypertensive state, and relatively specific to vasopressin. This withdrawal-induced antihypertensive phenomenon (WAP) does not appear to be due solely to the preceding natriuresis and diuresis during the infusion of vasopressin. However, because the hypertensive animal may be more sensitive to a given degree of sodium loss, the possibility that the natriuresis could play a contributing or permissive role cannot be excluded.
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PMID:Relationship of the antihypertensive effect of vasopressin withdrawal to sodium excretion in the Doca-salt hypertensive rat. 826 88