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

Zhang, Jin, W. Gil Wier, and Mordecai P. Blaustein. Mg2 blocks myogenic tone but not K -induced constriction: role for SOCs in small arteries. Am J Physiol Heart Circ Physiol 283: H2692–H2705, 2002. First published August 15, 2002; 10.1152/ajpheart.00260.2002.—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 M Nif. Contractions induced by 75 mM K depolarization were blocked by 0.3 M Nif, but not by 10 mM Mg2 . Phenylephrine (PE; 5 M) evoked sustained [Ca2 ]cyt elevation and vasoconstriction with superimposed Ca2 oscillations and vasomotion. The subsequent addition of 10 mM Mg2 or 0.3 M 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 1-adrenoceptorinduced tonic vasoconstriction.