This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jacob, H. J. Articles by Brody, M. J. Search for Related Content PubMed PubMed Citation Articles by Jacob, H. J. Articles by Brody, M. J.

Hypertension, Vol 14, 501-510, Copyright © 1989 by American Heart Association

ARTICLES

Lability of arterial pressure after baroreceptor denervation is not pressure dependent

HJ Jacob, RH Alper and MJ Brody
Department of Pharmacology, University of Iowa College of Medicine, Iowa City 52242.

The mechanisms of increased arterial pressure lability after sinoaortic deafferentation remain unknown. We have shown previously in rats with chronic sinoaortic deafferentation (7-14 days after sinoaortic deafferentation) that ganglionic blockade significantly reduced mean arterial pressure and arterial pressure lability. The present study investigated the possibility that lability is related to the level of arterial pressure. Rats were instrumented chronically and heart rate and mean arterial pressure were sampled every 5 seconds in the conscious, freely moving state. Graded sustained increases in pressure (+10 to +82 mm Hg) produced by constant infusion of angiotensin II, phenylephrine, or vasopressin did not affect lability (standard deviation of 30-minute sampling period); whereas, graded hypotension (- 10 to -70 mm Hg) produced by infusions of adenosine, nitroprusside, or nisoldipine appeared to reduce lability. Analysis of covariance and orthogonal polynomial curve fitting demonstrated a significant correlation between the decrease in mean arterial pressure and the decrease in lability produced by nisoldipine but not by adenosine or nitroprusside. Lability does not appear to be solely dependent on the level of arterial pressure because lability was reduced by adenosine when pressure was maintained at control levels by simultaneous infusion of phenylephrine. We conclude that 1) arterial pressure lability is not influenced by elevation of arterial pressure but can be reduced when pressure is lowered by certain vasodilators and 2) pressure alone does not appear to be the major determinant of lability because it can be attenuated by vascular smooth muscle relaxants even when pressure is maintained.

This article has been cited by other articles:

				G. F. DiBona and S. Y. Jones Dynamic Analysis of Renal Nerve Activity Responses to Baroreceptor Denervation in Hypertensive Rats Hypertension, April 1, 2001; 37(4): 1153 - 1163. [Abstract] [Full Text] [PDF]

				B. R. Dworkin, S. Dworkin, and X. Tang Carotid and aortic baroreflexes of the rat: I. Open-loop steady-state properties and blood pressure variability Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2000; 279(5): R1910 - R1921. [Abstract] [Full Text] [PDF]