Influence of intravenous and intracerebroventricular vasopressin on baroreflex control of renal nerve traffic.
We performed experiments in alpha-chloralose-anesthetized rabbits with vagi sectioned, to determine the influence of intravenous and intracerebroventricular vasopressin on arterial baroreflex control of renal nerve activity. Arterial baroreflex control of renal nerve activity was assessed during phenylephrine-induced increases and nitroglycerin-induced decreases in arterial pressure. Intravenous vasopressin (4 and 40 mU over 1 minute) reduced basal renal nerve activity (from 149 +/- 14 to 101 +/- 13 and 28 +/- 13 impulses/sec) without changing arterial pressure and reduced the sensitivity of the arterial baroreflex control of renal nerve activity. This effect was reversed by vasopressin antagonist (d(CH2)5[Tyr(Me)2]AVP) which blocks vasoconstrictor effects of vasopressin. Intracerebroventricular vasopressin (4, 40, or 400 mU) did not alter basal renal nerve activity or arterial pressure but increased the sensitivity of baroreflex control of renal nerve activity. This effect was not blocked by the vasopressin antagonist. The influence of intravenous vasopressin on basal renal nerve activity was not altered by sinoaortic baroreceptor denervation. In contrast, the inhibitory influence of intravenous vasopressin on lumbar sympathetic nerve activity was abolished by sinoaortic denervation. Finally, intravenous vasopressin inhibited renal nerve activity (by 43 +/- 5%) in six rabbits with spinal cord transection. This effect was abolished by the vasopressin antagonist. We draw the following conclusions from these data: (1) intravenous and intracerebroventricular vasopressin have different effects on basal and baroreflex control of renal nerve activity; (2) these effects are mediated by different vasopressin receptors; (3) the effects of intravenous vasopressin on basal renal nerve activity are not baroreflex dependent, and appear to be mediated by spinal or, possibly, ganglionic mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
- Copyright © 1986 by American Heart Association