EFFECT OF ANGIOTENSIN-II ON CALCIUM-RELEASE PHENOMENA IN NORMAL AND HYPERTROPHIED SINGLE CARDIAC MYOCYTES

The effects of angiotensin II (Ang II) (10(-9) M to 10(-7) M) on calci um releases were established in ventricular myocytes from normal and r enal hypertensive adult rats. From each peak systolic indo-1 ratio (40 5 nm/480 nm), amplitude variation, duration (rise time and fall time), and frequency of spontaneous calcium releases were investigated on fr eshly isolated cardiomyocytes at rest or under electrical stimulation. The following changes were observed: (1) in spontaneous contracting m yocytes, an increase in frequency of calcium transients at 10(-7) M in normal cells (+157%, P<0.05) and at whatever angiotensin II concentra tion in hypertrophied cells (10(-9) M: +79%, P<0.05; 10(-8) M +82%, P< 0.01; 10(-7) M: +285%, P<0.01) with a greater sensitivity of hypertrop hied cells to Ang II (P<0.05 at 10(-9) M, P<0.01 at 10(-8) M). (2) In stimulated myocytes, a prolongation of the duration of calcium transie nts at 10(-7) M in normal cells (+68%, P<0.01) and at 10(-9) M, 10(-8) M, 10(-7) M in hypertrophied cells: (+36%, P<0.05; +39%, P<0.01; +77% , P<0.01) with a greater sensitivity of hypertrophied myocytes (P<0.05 at 10(-9) M and 10(-8) M). An increase in duration may be explained b y the occurrence of calcium releases during the fall time of calcium t ransients. Thus, both in normal and hypertrophied myocytes, Ang II ind uced the occurrence of calcium releases with increased sensitivity of hypertrophied cells to Ang IT. Such calcium releases are known to be a possible cause of arrhythmias termed ''triggered activity''.