Excitation-contraction coupling in ventricular myocytes: effects of angiotensin II

The effects of the vasoactive peptide angiotensin II (AII) on contractility and excitation-contraction coupling in isolated adult rabbit ventricular myocytes were investigated. In most ventricular myocytes, AII (10(-8) M) induced a significant increase in fractional shortening which was not associated with an increase in the calcium transient measured with indo-1. AII did increase the intracellular pH by approximately 0.2 5 pH units coincident with the positive inotropic effect. Effects of AII on pH and contractility were blocked by inhibitors of Na+/H+ exchange. AII also increased the rate of pHi recovery from intracellular acidosis at pHi values above 6.9. AII was shown not to affect the L-type inward calcium current. However, in an occasional cell, AII was observed to cause a slight increase in the calcium transient. We hypothesize that this response may reflect an increase of calcium influx on the sodium calcium exchanger, as a consequence of an increase in subsarcolemmal sodium concentration resulting from enhanced Na(+)-H+ exchange.