Slowing of ca2+ transient decline is an early manifestation of
pressure-overload hypertrophy in rat hearts.
Chang, Kevin C., Joop H. M. Schreur, Michael W. Weiner, and S. Albert
Camacho.
Departments of Medicine and Radiology, and Cardiovascular Research
Institute, University of California, San Francisco, CA 94143, and the
Magnetic Resonance Unit, Department of Veterans Affairs Medical
Center, San Francisco, CA 94121, and the Department of Medicine
(Cardiology), San Francisco General Hospital, San Francisco, CA
94110
APStracts 2:0552H, 1995.
Both cytosolic free Ca2+ ([Ca2+]c) decline and myocardial relaxation
are slowed in severe hypertrophy and heart failure. However, it is
not certain whether this occurs in mild to moderate hypertrophy.
Therefore, we tested the hypotheses that slowing of [Ca2+]c decline:
1) occurs in mild to moderate hypertrophy, 2) occurs in the absence
of slowed relaxation, and 3) is related to the degree of hypertrophy.
Experiments were performed on isolated rat hearts subjected to
pressure-overload. Indo-1 fluorescence was used as an index of
[Ca2+]c. [Ca2+]c decline and myocardial relaxation were assessed by
the time constant of exponential [Ca2+]c decline (tCa) and LV
pressure decline (tP), respectively. Mean tCa was significantly
increased in hearts from banded rats compared to sham-operated rats
(59 +/- 13 vs. 45 +/- 5 ms, p = 0.03). In contrast, there was no
difference in mean tP (28 +/- 3 vs. 29 +/- 5 ms, p = NS). There was a
linear relationship between tCa and LV dry weight (r = 0.79). In
summary, slowing of the [Ca2+]c transient decline occurred in mild to
moderate hypertrophy. However, LV relaxation was unaffected.
Furthermore, slowing of the [Ca2+]c transient decline was closely
related to the degree of LV hypertrophy. These data suggest that
slowing of [Ca2+]c decline is an early manifestation of pressure
-overload hypertrophy that precedes slowing of relaxation.
Received 20 September 1994; accepted in final form 30 November
1995
APS Manuscript Number H846-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 12 December 95