Ca2+ transients in hypertensive and post-infarction myocytes. Zhang, Xue-Qian, Russell L. Moore, Thomas Tenhave, and Joseph Y. Cheung. Departments of Medicine, and Cellular and Molecular Physiology, and Center for Biostatistics and Epidemiology, Milton S. Hershey Medical Center, The Pennsylvania State University, Hershey, Pennsylvania 17033
APStracts 2:0142C, 1995.
Frequency dependence of stimulated changes in intracellular calcium ([Ca2+]i) in single left ventricular (LV) myocytes isolated from Sham, renovascular hypertensive (HYP) and myocardial infarcted (MI) rats was examined. [Ca2+]i in fura-2 loaded myocytes was measured using a modified single wavelength method. Increasing pacing frequency progressively from 0.1 to 5Hz increased both systolic and diastolic [Ca2+]i in myocytes from all groups. Compared with their age-matched controls, HYP myocytes paced at physiological rates had similar systolic but elevated diastolic [Ca2+]i. By contrast, systolic [Ca2+]i was slightly but significantly lower and diastolic [Ca2+]i significantly higher in MI myocytes when compared with their appropriate controls. These observations suggest that HYP and MI induced distinctly different changes in Ca2+ regulatory mechanisms and that the different patterns of alterations in [Ca2+]i dynamics may partly explain predominantly diastolic dysfunction in hypertensive hypertrophic hearts and systolic dysfunction in hearts surviving MI. In the presence of 1[mu]M isoproterenol, both HYP and MI myocytes had much lower systolic [Ca2+]i when compared with their respective controls. Isoproterenol restored the elevated diastolic [Ca2+]i in HYP myocytes towards normal, but had no effect on the intrinsic differences in diastolic [Ca2+]i between Sham and MI myocytes. These observations are consistent with the hypothesis that [beta]-adrenergic responsiveness is decreased in hypertrophied ventricles induced by chronic pressure overload or MI, or alternatively isoproterenol affects different Ca2+ regulatory pathways to different degrees in these two models of cardiomyopathy. The observation that isoproterenol lowers diastolic [Ca2+]i in HYP myocytes towards normal may provide a cellular mechanism for the lack of efficacy of [beta]-adrenergic blockers to improve diastolic compliance in patients with hypertensive hypertrophic cardiomyopathy. 

Received 8 November 1994; accepted in final form 3 March 1995.
APS Manuscript Number C664-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 28 March 1995.