Pressor response to vasopressin and impaired baroreflex function in DOC-salt hypertension.
Baroreflexes and pressor responses to intravenous arginine vasopressin (AVP) and phenylephrine (PE) were evaluated in conscious, less severely hypertensive desoxycorticosterone (DOC)-salt-treated rats, hypertensive DOC-salt-treated rats, and control rats (n = 6, each group). Pressor responses were retested after ganglionic blockade. In control rats pressor responses to AVP were augmented more than those to PE after ganglion blockade; thus AVP appeared uniquely to augment baroreflex buffering. In hypertensive DOC-salt-treated rats baroreflexes were impaired (P less than 0.05); pressor responsiveness to AVP was augmented compared with control rats (P less than 0.05). After ganglion blockade augumentation of pressor responses was similar for AVP and PE. In less severely hypertensive rats baroreflexes were normal; pressor responses to AVP and PE were like those in control rats before and after ganglion blockade. These results suggest that AVP augments baroreflex buffering, which imposes a restraint on pressor effects of AVP that is not evident with PE. In hypertensive DOC-salt-treated rats a defect in baroreflex buffering during infusion of AVP may contribute to augmented pressor effects of AVP.
D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood / Q000494:pharmacology*; D003900:Desoxycorticosterone; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D009392:Nephrectomy; D010656:Phenylephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride
D001127:Arginine Vasopressin; D010656:Phenylephrine; D003900:Desoxycorticosterone; D012965:Sodium Chloride