Chronic angii infusion resets reflex control of norepinephrine and
corticosterone by a pressure-independent mechanism.
Brooks, Virginia L., and Daniel C. Hatton.
Departments of Physiology and Behavioral Neuroscience, The Oregon
Health Sciences University, Portland, Oregon 97201-3098, (503) 494
-5843, FAX: (503) 494-4352
APStracts 3:0308R, 1996.
The hypothesis that long-term increases in angiotensin II (AII)
produce pressure-independent resetting of baroreflex control of the
sympathetic nervous system and the hypothalamo-pituitary adrenal axis
was tested in rabbits by determining the effect of chronic AII
infusion on reflex relationships between arterial pressure (MAP) and
plasma concentrations of norepinephrine (NE) and corticosterone (CS).
After 2 weeks, AII increased MAP from 61+/-1 to 99+/-2 mmHg
(p<0.05) without altering heart rate or plasma NE concentration,
but increased CS from 9.8+/-1.3 to 29.5+/-13.7 ng/ml (p<0.05).
Heart rate, NE and CS baroreflex curves were all reset to a higher
pressure level (p<0.05) after 24 hr, 1 wk and 2 wk of AII. Forty
min after stopping AII on the same days, MAP decreased, and curves
were shifted back toward control (p<0.05), indicating that AII
was required for the resetting. Two findings suggest that the
resetting action of AII is distinct from the pressor effect. First,
while stopping AII reversed the hypertension as it reversed the
resetting, reversal of the hypertension instead by prolonged infusion
of nitroprusside along with AII did not have the same effect. Second,
NE and heart rate baroreflex curves returned toward pre-infusion
positions after stopping AII (p<0.05), even when the
hypertension was nearly maintained by phenylephrine infusion. In
conclusion, chronic increases in AII may have a global baroreflex
resetting effect by a mechanism that is in part independent of the
hypertension.
Received 14 May 1996; accepted in final form 25 July 1996.
APS Manuscript Number R270-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996