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Departments of Radiology and Medicine (Cardiology), University of California, San Francisco 94143; and the Medical Service, San Francisco General Hospital, San Francisco, California 94110
The goal of this
study was to determine whether
Ca2+ plays a role in regulating
tension development kinetics in intact cardiac muscle. In cardiac
muscle, this fundamental issue of
Ca2+ regulation has been
controversial. The approach was to induce steady-state tetanic
contractions of intact right ventricular trabeculae from rat hearts at
varying external Ca2+
concentrations
([Ca2+]) at 22°C.
During tetani, cross bridges were mechanically disrupted and the kinetics of tension redevelopment were assessed from the rate
constant of exponential tension redevelopment
(ktr). There was a relationship between
ktr and external
[Ca2+] that was
similar in form to the relationship between tension and
[Ca2+]. Thus a close
relationship also existed between
ktr and tension (r = 0.88;
P < 0.001); whereas at
maximal tetanic tension (saturating cytosolic
[Ca2+]),
ktr was 16.4 ± 2.2 s
1 (mean ± SE, n = 7), at zero tension (low
cytosolic [Ca2+]),
ktr extrapolated
to 20% of maximum (3.3 ± 0.7 s1). Qualitatively
similar results were obtained using different mechanical protocols to
disrupt cross bridges. These data demonstrate that tension
redevelopment kinetics in intact cardiac muscle are influenced by the
level of Ca2+ activation. These
findings contrast with the findings of one previous study of intact
cardiac muscle. Activation dependence of tension development kinetics
may play an important role in determining the rate and extent of
myocardial tension rise during the cardiac cycle in vivo.
cross-bridge kinetics; activation; rate constant of exponential tension redevelopment; contraction; trabeculae
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