Hypertension alters rapid cooling contractures in single rat cardiocytes.
Previous work has demonstrated that, in single, paced left ventricular (LV) myocytes isolated from rats with hypertension, the extent of myocyte shortening and the amplitude of the cytosolic Ca2+ concentration transient are decreased relative to normal myocytes. These findings suggest that reduced sarcoplasmic reticular (SR) Ca2+ release could be responsible for hypertension-induced attenuation of the myocyte contractile response. Hypertension-induced reductions in SR Ca2+ release could be due to 1) a decrease in releasable SR Ca2+ content relative to the sarcoplasmic volume into which it is released or 2) alterations in the SR Ca2+ release mechanism such that the fractional release of SR Ca2+ is reduced. Using rapid cooling contractures (RCCs) to provide an index of SR Ca2+ content, we conducted a series of experiments designed to test the former hypothesis. Single LV myocytes were isolated from normotensive control rats and from rats with hypertension, which was induced by abdominal aortic banding (for approximately 4 mo). The extent of myocyte shortening during an RCC is taken to be directly proportional to SR Ca2+ content. As expected, the amplitudes of both twitches and RCCs decreased as pacing frequency increased from 0.2 to 1.0 Hz across both control and hypertensive groups, although the effect was greatest in control myocytes. A significant finding of this study was that, at both pacing frequencies, RCC magnitude was attenuated in hypertensive relative to control myocytes. These results suggest that in hypertension cellular Ca2+ homeostasis is altered and there is a mismatch between releasable SR Ca2+ content and the sarcoplasmic volume into which it is released.