AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol (December 22, 2004). doi:10.1152/ajpheart.01069.2004
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Submitted on October 19, 2004
Accepted on December 20, 2004

Decreased Ca extrusion via Na/Ca exchange in epicardial left ventricular myocytes during compensated hypertrophy

Mark R Fowler1, James R Naz1, Mark D Graham1, Gilles Bru-Mercier1, Simon M Harrison1, and Clive H Orchard1*

1 School of Biomedical Sciences, University of Leeds, Leeds, West Yorkshire, United Kingdom

* To whom correspondence should be addressed. E-mail: c.h.orchard{at}leeds.ac.uk.

Hypertension-induced cardiac hypertrophy alters the amplitude and time course of the systolic Ca2+ transient of sub-epicardial and sub-endocardial ventricular myocytes. The present study was designed to elucidate the mechanisms underlying these changes. Myocytes were isolated from the left ventricular sub-epicardium and sub-endocardium of 20 week-old spontaneously hypertensive (SHR) and age-matched normotensive Wistar Kyoto (WKY; control) rats. Ca2+i was monitored using fluo-3 or fura-2; caffeine (20 mmol.L-1) was used to release Ca2+ from the sarcoplasmic reticulum (SR), and Ni2+ (10 mM) to inhibit Na/Ca exchange (NCX) function. SHR myocytes were significantly larger than those from WKY hearts, consistent with cellular hypertrophy. Subepicardial myocytes from SHR hearts showed larger Ca2+ transient amplitude, SR Ca2+ content and less Ca2+ extrusion via NCX, compared to sub-epicardial WKY myocytes. These parameters did not change in sub-endocardial myocytes. The time course of decline of the Ca2+ transient was the same in all groups of cells, but its time to peak was shorter in sub-epicardial cells than in sub-endocardial cells in WKY and SHR, and was slightly prolonged in sub-endocardial SHR cells compared to WKY sub-endocardial myocytes. It is concluded that the major change in Ca2+ cycling during compensated hypertrophy in SHR is a decrease in NCX activity in sub-epicardial cells; this increases SR Ca2+ content and hence Ca2+ transient amplitude, thus helping to maintain the strength of contraction in the face of an increased afterload.




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