TY - JOUR
T1 - Excitation-contraction coupling in ventricular myocytes
T2 - Effects of angiotensin II
AU - Barry, W. H.
AU - Matsui, H.
AU - Bridge, J. H.B.
AU - Spitzer, K. W.
AU - Janicki, J.
AU - O'Rourke, B.
AU - Kessler-Icekson, G.
AU - Morad, M.
PY - 1995
Y1 - 1995
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0029089474&partnerID=8YFLogxK
U2 - 10.1007/978-1-4615-1893-8_4
DO - 10.1007/978-1-4615-1893-8_4
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C2 - 8540409
AN - SCOPUS:0029089474
SN - 0065-2598
VL - 382
SP - 31
EP - 39
JO - Advances in Experimental Medicine and Biology
JF - Advances in Experimental Medicine and Biology
ER -