AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 283: H2692-H2705, 2002. First published August 15, 2002; doi:10.1152/ajpheart.00260.2002
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Vol. 283, Issue 6, H2692-H2705, December 2002

Mg2+ blocks myogenic tone but not K+-induced constriction: role for SOCs in small arteries

Jin Zhang, W. Gil Wier, and Mordecai P. Blaustein

Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201

The effects of Mg2+ and nifedipine (Nif) on vasoconstriction and Ca2+ transients were studied in intact, pressurized rat mesenteric arteries with myogenic tone. Changes in cytosolic Ca2+ concentration ([Ca2+]cyt) were measured with confocal microscopy in fluo 4-AM loaded, individual myocytes. Myogenic tone was abolished by 10 mM Mg2+ or 0.3 µM Nif. Contractions induced by 75 mM K+ depolarization were blocked by 0.3 µM Nif, but not by 10 mM Mg2+. Phenylephrine (PE; 5 µM) evoked sustained [Ca2+]cyt elevation and vasoconstriction with superimposed Ca2+ oscillations and vasomotion. The subsequent addition of 10 mM Mg2+ or 0.3 µM Nif reduced [Ca2+]cyt and abolished plateau vasoconstriction. When added before PE, both Mg2+ and Nif abolished the PE-evoked Ca2+ oscillations and vasomotion. Mg2+ dilated the PE-constricted arteries after a brief (<= 180-240 s) vasoconstriction, but Nif did not. Both agents also abolished the vasoconstriction attributed to Ca2+ entry through store-operated channels (SOCs) during internal Ca2+ store refilling that followed store depletion. The data suggest that Ca2+ entry through SOCs helps maintain both myogenic tone and alpha 1-adrenoceptor-induced tonic vasoconstriction.

confocal laser scanning microscopy; nifedipine; cytosolic Ca2+ concentration; phenylephrine; mesenteric artery


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