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

W. H. Barry*, H. Matsui, J. H.B. Bridge, K. W. Spitzer, J. Janicki, B. O'Rourke, G. Kessler-Icekson, M. Morad

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


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 pH(i) 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.

Original languageEnglish
Pages (from-to)31-39
Number of pages9
JournalAdvances in Experimental Medicine and Biology
StatePublished - 1995
Externally publishedYes


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