Vasopressin-induced increase in total peripheral resistance in deoxycorticosterone acetate hypertensive rats is buffered by the baroreceptor reflex.

Abstract

1. The role of arginine-vasopressin (AVP) in the maintenance of high blood pressure in rats with deoxycorticosterone acetate (DOCA) hypertension was investigated. 2. Plasma concentrations of AVP were significantly elevated in DOCa hypertensive rats compared with normotensive control rats, whether or not they received 1% sodium chloride solution or demineralized water to drink. 3. The specific antagonist of the vasopressor response to AVP, d(CH2)5VDAVP (100 microgram/kg intravenously), significantly increased cardiac output and decreased total peripheral resistance, but had no effect on mean arterial pressure in DOCA hypertensive rats. No changes of mean arterial pressure, cardiac output and total peripheral resistance were observed in the normotensive control groups after d(CH2)5VDAVP. 4. After sino-aortic baroreceptor deafferentation, d(CH2)5VDAVP decreased mean arterial pressure in DOCA--salt hypertensive rats, but not in the control groups. 5. It is concluded that elevated circulating AVP causes vasoconstriction in DOCA hypertensive rats. The AVP-induced increase in total peripheral resistance is counter-regulated by an activation of the baroreceptor reflex and subsequent reduction in cardiac output.