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

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 muM Nif Contractions induced by 75 mM K+ depolarization were blocked by 0.3 muM Nif, but not by 10 mM Mg2+. Phenylephrine (PE; 5 muM) evoked sustained [Ca2+](cyt) elevation and vasoconstriction with superimposed Ca2+ oscillations and vasomotion. The subsequent addition of 10 mM Mg2+ or 0.3 muM 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 (less than or equal to 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.