© 2001 American Heart Association, Inc.
Integrative Physiology |
Reverse Mode of the Na+-Ca2+ Exchange After Myocardial Stretch
Underlying Mechanism of the Slow Force Response
From the Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata, Argentina.
Correspondence to Dr Horacio E. Cingolani, Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, UNLP, 60 y 120 (1900) La Plata, Argentina. E-mail cicme{at}atlas.med.unlp.edu.ar
Abstract—This
study was designed to gain additional insight into the mechanism of the
slow force response (SFR) to stretch of cardiac muscle. SFR and changes
in intracellular Na+ concentration
([Na+]i) were
assessed in cat papillary muscles stretched from 92% to 
98% of
Lmax. The SFR was 120±0.6% (n=5) of the rapid
initial phase and coincided with an increase in
[Na+]i. The SFR was
markedly depressed by
Na+-H+ exchanger
inhibition, AT1 receptor blockade, nonselective
endothelin-receptor blockade and selective
ETA-receptor blockade, extracellular
Na+ removal, and inhibition of the reverse
mode of the
Na+-Ca2+ exchange
by KB-R7943. KB-R7943 prevented the SFR but not the increase in
[Na+]i. Inhibition
of endothelin-converting enzyme activity by phosphoramidon suppressed
both the SFR and the increase in
[Na+]i. The SFR and
the increase in
[Na+]i after
stretch were both present in muscles with their endothelium (vascular
and endocardial) made functionally inactive by Triton X-100. In these
muscles, phosphoramidon also suppressed the SFR and the increase in
[Na+]i. The data
provide evidence that the last step of the autocrine-paracrine
mechanism leading to the SFR to stretch is
Ca2+ entry through the reverse mode of
Na+-Ca2+
exchange.
Key Words: myocardial stretch • Na+-Ca2+ exchange • Na+-H+ exchange • angiotensin II • endothelin
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