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AJP - Heart and Circulatory Physiology, Vol 259, Issue 3 712-H719, Copyright © 1990 by American Physiological Society
ARTICLES |
F. Kolar, W. C. Cole, B. Ostadal and N. S. Dhalla
Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada.
The inotropic effects of low concentrations of extracellular Na+ (35-110 mM) were studied using Langendorff-perfused rat hearts. Low Na+ induced an initial positive inotropic response proportional to the decrease of transsarcolemmal Na+ gradient. At 35 mM Na+, this effect was followed by a secondary fall in contractility and rise of resting force (RF) and then by a delayed positive inotropic effect and recovery of RF. The magnitude of these low Na(+)-induced transient changes was dependent on the extracellular Ca2+ concentration and was altered by amiloride (6 x 10(-4) and 2.5 x 10(-3) M), ouabain (5 x 10(-5) and 5 x 10(-4) M), ryanodine (2 x 10(-8), 1 x 10(-7) and 1 x 10(-6) M), and sodium azide (1 x 10(-3) and 5 x 10(-3) M) but not by verapamil (2 x 10(-8) and 1 x 10(-7) M) or vanadate (4 x 10(-6) M). The data indicate the initial positive inotropic response of the rat heart to low Na+ may be due to rapid loading of myocytes with Ca2+ through the Na(+)-Ca2+ exchange mechanism. The secondary depression of contractility and the rise of RF appear to be the consequence of the short-lived intracellular Ca2+ overload. Furthermore, the recovery of contractions and the delayed positive inotropic response may be the result of the intracellular redistribution of excessive Ca2+ into the sarcoplasmic reticulum with mitochondria and increased transsarcolemmal Ca2+ efflux apparently playing a more minor role.
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H. K. Saini and N. S. Dhalla Modification of intracellular calcium concentration in cardiomyocytes by inhibition of sarcolemmal Na+/H+ exchanger Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2790 - H2800. [Abstract] [Full Text] [PDF] |
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