Contributions of Vasopressin and Other Pressor Systems to DOC-Salt Hypertension in Rats

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Abstract
The roles of arginine vasopressin (AVP), the sympathetic nervous system and the renin-angiotensin system in maintaining elevated blood pressure in established DOC[deoxycorticosterone]-salt hypertension in rats were studied by injection of specific antagonists of these systems. The specific AVP antagonist dPVDAVP [d(CH2)5Tyr(Methyl)AVP] decreased blood pressure by 19 .+-. 3 mm Hg in hypertensive rats and 6 .+-. 2 mm Hg in control rats. In a different group of rats ganglionic blockade with chlorisondamine also caused a greater decrease in blood pressure in DOC-salt rats compared to controls (99 .+-. 6 vs. 58 .+-. 4 mm Hg, respectively). In rats with autonomic ganglia blocked subsequent vasopressin antagonism decreased blood pressure 29 .+-. 4 mm Hg in DOC-salt rats and 14 .+-. 2 mm Hg in control rats. Converting enzyme inhibition with captopril in rats with autonomic ganglia blocked caused a lesser decrease in blood pressure in DOC-salt rats than in controls (8 .+-. 2 vs. 14 .+-. 2 mm Hg, respectively). Both AVP and the sympathetic nervous system contribute to the maintenance of DOC-salt hypertension. The renin-angiotensin system appears to be relatively less important.

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