Catecholamine response to chronic angiotensin ii infusion and its
role in myocyte and coronary vascular damage.
Henegar, Jeffrey R., Gregory L. Brower, Ameer Kabour, Joseph S.
Janicki.
Department of Internal Medicine and Dalton Cardiovascular Research
Center, University of Missouri, Columbia, Missouri, U.S.A.
APStracts 2:0178H, 1995.
Acute elevations in circulating angiotensin II (AngII) are known to
increase circulating norepinephrine (NE) levels. However, the time
-course of catecholamine release relative to chronic AngII infusion is
not known. Furthermore, it is unknown if this AngII-induced
catecholamine release is AngII type 1 (AT1 ) receptor mediated and
whether the increase in serum catecholamines is responsible for the
myocyte and coronary vascular damage seen within the first 3 days of
chronic AngII infusion. Therefore, we examined the influence of
chronic AngII stimulation on serum catecholamine levels with and
without AT1 blockade and the effect of -blockade on AngII-induced
myocyte and coronary vascular damage. The results indicate that NE
release is AT1 mediated, but NE is not significantly elevated until
day 4 of AngII infusion after which it remains elevated. blockade
prevented most AngII related myocyte necrosis and coronary vascular
damage. Therefore, myocyte and coronary vascular damage do not appear
to be related to increased serum NE levels but instead may be due to
the release of neural catecholamines within the heart.
Received 15 February 1995; accepted in final form 24 April 1995.
APS Manuscript Number H142-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 9 May 1995.