Effects of adenosine and protein kinase c stimulation on mechanical
properties of rat cardiac myocytes.
Lester, J. W., K. F. Gannaway, R. A. Reardon, L. D. Koon, and P. A.
Hofmann.
Department of Physiology and Biophysics, College of Medicine,
University of Tennessee, Memphis
APStracts 3:0112H, 1996.
Exposure of the heart to adenosine decreases heart rate and left
ventricular developed pressure. However, little is known regarding
the influence of adenosine on mechanical properties of isolated
ventricular myocytes and the intracellular mechanism(s) by which
adenosine acts. Therefore in the present study we compared the
effects of the adenosine receptor agonist R-phenylisopropyladenosine
(R-PIA) and protein kinase C activator dioctanoylglycerol (DOG) on
Ca2+ sensitivity of tension, maximum isometric tension, and velocity
of unloaded shortening (Vmax) in enzymatically isolated, drug
treated, and subsequently skinned ventricular myocytes. Neither R-PIA
(100 [mu]M) nor DOG (50 [mu]M) affected Ca2+ sensitivity of tension
or maximum isometric tension as compared to controls. However, both
R-PIA and DOG treatment caused an approximate 25% decrease in Vmax
during maximum activation as compared to controls. This suggests
adenosine and PKC decrease actin-myosin interaction through an
alteration of myofilament proteins. The observed similarity of
response following R-PIA and DOG treatment is consistent with the
hypothesis that effects of adenosine are mediated by activation of
the protein kinase C pathway in isolated ventricular myocytes.
Received 10 November 1995; accepted in final form 6 March 1996.
APS Manuscript Number H1057-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96