[Ca2+]i transients in hypertensive and postinfarction myocytes.

Changes in intracellular calcium concentration ([Ca2+]i) in paced fura 2-loaded myocytes isolated from Sham, renovascular hypertensive (Hyp), and myocardial-infarcted (MI) rats were examined. Compared with controls, Hyp myocytes paced at physiological rates had similar systolic but elevated diastolic [Ca2+]i. By contrast, systolic [Ca2+]i was significantly lower and diastolic [Ca2+]i higher in MI myocytes. The different patterns of alterations in [Ca2+]i dynamics in Hyp and MI myocytes may partly explain predominantly diastolic dysfunction in hypertensive hearts and systolic dysfunction in hearts surviving MI. In the presence of 1 microM 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 toward normal but had no effect on the intrinsic differences in diastolic [Ca2+]i between Sham and MI myocytes. The observation that isoproterenol lowers diastolic [Ca2+]i in Hyp myocytes toward 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.