Differential changes in left and right ventricular adenylyl cyclase
activities in congestive heart failure.
Sethi, Rajat, Ken S. Dhalla, Robert E. Beamish, and Naranjan S.
Dhalla.
Institute of Cardiovascular Sciences, St. Boniface General Hospital
Research Centre and Department of Physiology, Faculty of Medicine,
University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6
APStracts 3:0403H, 1996.
The status of [beta]-adrenoceptors and adenylyl cyclase in crude
membranes from both left and right ventricles was examined upon
occluding the left coronary artery in rats for 4, 8 and 16 weeks. The
adenylyl cyclase activity in the presence of isoproterenol was
decreased in the uninfarcted (viable) left ventricle and increased in
the right ventricle subsequent to myocardial infarction. The density
of [beta]1-adrenoceptors, unlike [beta]2-receptors, was reduced in
the left ventricle whereas no change in the characteristics of
[beta]1- and [beta]2-adrenoceptors was seen in the right ventricle.
The catalytic activity of adenylyl cyclase was depressed in the
viable left ventricle but was unchanged in the right ventricle. In
comparison to sham controls, the basal, as well as NaF-, forskolin-,
and Gpp(NH)p-stimulated adenylyl cyclase activities, were decreased
in the left ventricle and increased in the right ventricle of the
experimental animals. Opposite alterations in the adenylyl cyclase
activities in left and right ventricles from infarcted animals were
also seen when two types of purified sarcolemmal preparations were
employed. These changes in adenylyl cyclase activities in the left
and right ventricles were dependent upon the degree of heart failure.
Furthermore, cyclic AMP contents were higher in the right ventricle
and lower in the left ventricle from infarcted animals injected with
saline, isoproterenol or forskolin in comparison to the controls. The
results suggest differential changes in the viable left and right
ventricles with respect to adenylyl cyclase activities during the
development of congestive heart failure due to myocardial infarction.
Received 23 August 1995; accepted in final form 9 September 1996.
APS Manuscript Number H799-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 7 October 1996