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Decreased Ca²⁺ extrusion via Na⁺/Ca²⁺ exchange in epicardial left ventricular myocytes during compensated hypertrophy

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

Submitted 19 October 2004 ; accepted in final form 20 December 2004

Hypertension-induced cardiac hypertrophy alters the amplitude and time course of the systolic Ca²⁺ transient of subepicardial and subendocardial ventricular myocytes. The present study was designed to elucidate the mechanisms underlying these changes. Myocytes were isolated from the left ventricular subepicardium and subendocardium of 20-wk-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY; control). We monitored intracellular Ca²⁺ using fluo 3 or fura 2; caffeine (20 mmol/l) was used to release Ca²⁺ from the sarcoplasmic reticulum (SR), and Ni²⁺ (10 mM) was used to inhibit Na⁺/Ca²⁺ 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 and SR Ca²⁺ content and less Ca²⁺ extrusion via NCX compared with subepicardial WKY myocytes. These parameters did not change in subendocardial 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 subepicardial cells than in subendocardial cells in WKY and SHR and was slightly prolonged in subendocardial SHR cells compared with WKY subendocardial myocytes. It is concluded that the major change in Ca²⁺ cycling during compensated hypertrophy in SHR is a decrease in NCX activity in subepicardial 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.

cardiac myocytes; epicardium; endocardium; sarcoplasmic reticulum; t tubules; spontaneously hypertensive rats

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