AJP - Cell Physiology, Vol 262, Issue 4 C980-C990, Copyright © 1992 by American Physiological Society
Relaxation abnormalities in single cardiac myocytes from renovascular hypertensive rats
R. V. Yelamarty, R. L. Moore, F. T. Yu, M. Elensky, A. M. Semanchick and J. Y. Cheung
Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.
In myocardial hypertrophy secondary to renovascular hypertension, the rate
of intracellular Ca2+ concentration decline during relaxation in paced left
ventricular (LV) myocytes isolated from hypertensive (Hyp) rats is much
slower compared with that from normotensive (Sham) rats. By use of a novel
liquid-crystal television-based optical-digital processor capable of
performing on-line real-time Fourier transformation and the striated
pattern (similar to 1-dimensional diffraction grating) of cardiac muscle
cells, sarcomere shortening and relaxation velocities were measured in
single Hyp and Sham myocytes 18 h after isolation. There were no
differences in resting sarcomere length, percent of maximal shortening,
time to peak shortening, and average sarcomere shortening velocity between
Sham and Hyp cardiac cells. In contrast, average sarcomere relaxation
velocity and half-relaxation time were significantly prolonged in Hyp
myocytes. Contractile differences between Sham and Hyp myocytes detected by
the optical-digital processor are confirmed by an independent method of
video tracking of whole cell length changes during excitation-contraction.
Despite the fact that freshly isolated myocytes contract more rigorously
than 18-h-old myocytes, the relaxation abnormality was still observed in
freshly isolated Hyp myocytes, suggesting impaired relaxation is an
intrinsic property of Hyp myocytes rather than changes brought about by
short-term culture. We postulate that reduced sarcomere relaxation velocity
is a direct consequence of impaired Ca2+ sequestration-extrusion during
relaxation in Hyp myocytes and may be responsible for diastolic dysfunction
in hypertensive hypertrophic myocardium at the cellular level.
