Calcium Current in Normal and Hypertrophied Isolated Rat Ventricular Myocytes

Abstract

Chronic overloading of the heart induces hypertrophy of the myocardium leading to structural, biochemical and functional alterations of the myocardial cells (1). Prolonged action potential duration is a general property of the hypertrophied hearts in different species (2,3,4). Action potentials (AP) recorded in cat papillary muscles, after pulmonary banding, shows marked alterations: a slow rate of rise associated with a slow conduction and an increase in duration (5). It was further described that AP prolongation and depressed plateau were more visible with larger hypertrophy and at moderate hypertrophy with higher stimulation frequency (6). Similar changes were reported in the hypertrophied right ventricle of the rabbit (7). In the left ventricle of the rat, prolonged AP (9) were also observed whatever hypertrophy was induced following renal hypertension (8) or abdominal aortic stenosis (9). Experimental hypertrophy is more marked in the epicardium than in the endocardium in the Goldblatt rats (10). This is associated with more durable AP in the ventricular trabeculum than in the papillary muscle (11). Among the many experimental conditions, only volumetric overloading which can induce up to 80% hypertrophy was not associated with prolonged AP (9). Natural hypertrophy, as during genetic cardiomyopathy, also shows an increase in AP duration both in the Syrian hamster (12) and the human (13).