Contractile properties of left ventricular myocytes isolated from spontaneously hypertensive rats

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Abstract
Objective This study was undertaken to clarify whether the myocardial dysfunction observed in the hypertensive heart is an intrinsic property of the myocyte or not. Materials and methods We investigated left ventricular function and contractile function of myocytes from 30-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We also evaluated the effect of angiotensin II on contractile function of myocytes from both rats. Results The time constant of isovolumic pressure fall was significantly greater in SHR (13.2±0.6 ms) than in WKY (10.3±0.5 ms). The extent of shortening in isolated myocytes was significantly higher in SHR (11.3±0.4%) than in WKY (9.8±0.4%, P<0.01). Both the normalized maximal velocity of shortening and the normalized maximal velocity of relengthening were significantly greater in SHR (2.12±0.08 and 2.10±0.08s-1; both P<0.01) than in WKY (1.76±0.06 and 1.75±0.07s-1). Angiotensin II caused significant decreases in the extent of shortening, the normalized maximal velocity of shortening and the normalized maximal velocity of relengthening in isolated myocytes from SHR, but these parameters were unchanged in WKY. Conclusions These results suggest that left ventricular diastolic dysfunction in SHR is not due to an intrinsic abnormality of the cardiac myocytes, and that angiotensin II suppresses the function of myocytes from hypertrophied hearts.

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