Hypertension alters rapid cooling contractures in single rat
cardiocytes.
Stauffer, Brian L., Bradley M. Palmer, Alexander Hazel, Joseph Y.
Cheung, and Russell L. Moore.
Department of Kinesiology, Campus Box 354, University of Colorado,
Boulder, C0 80309-0354 & The Department of Medicine, Division of
Nephrology, The Pennsylvania State University College of Medicine,
P.O. Box 850, Hershey, PA 17033
APStracts 3:0362C, 1996.
Previous work has demonstrated that in single, paced left ventricular
(LV) myocytes isolated from rats with hypertension (HTN), the extent
of myocyte shortening and the amplitude of the cytosolic [Ca2&]
transient are decreased relative to normal myocytes. These findings
suggest that reduced sarcoplasmic reticular (SR) Ca2& release
could be responsible for HTN-induced attenuation of the myocyte
contractile response. HTN-induced reductions in SR Ca2& release
could be due to (i) a decrease in releasable SR Ca2& content
relative to the sarcoplasmic volume into which it is released or (ii)
to 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 (C) and from rats with hypertension (HTN) that was
induced by abdominal aortic banding (for 4 months). The extent of
myocyte shortening during a 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 C and HTN groups, although the effect was greatest in C
myocytes. A significant finding of this study was that at both pacing
frequencies, RCC magnitude was attenuated in HTN relative to C
myocytes. These results suggest that in HTN, cellular Ca2&
homeostasis is altered and that there is a mismatch between
releasable SR Ca2& content and the sarcoplasmic volume into which
it is released.
Received 1 December 1995; accepted in final form 26 September
1996.
APS Manuscript Number C721-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996