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

The effects of Mg(2+) and nifedipine (Nif) on vasoconstriction and Ca(2+) transients were studied in intact, pressurized rat mesenteric arteries with myogenic tone. Changes in cytosolic Ca(2+) concentration ([Ca(2+)](cyt)) were measured with confocal microscopy in fluo 4-AM loaded, individual myocytes. Myogenic tone was abolished by 10 mM Mg(2+) or 0.3 microM Nif. Contractions induced by 75 mM K(+) depolarization were blocked by 0.3 microM Nif, but not by 10 mM Mg(2+). Phenylephrine (PE; 5 microM) evoked sustained [Ca(2+)](cyt) elevation and vasoconstriction with superimposed Ca(2+) oscillations and vasomotion. The subsequent addition of 10 mM Mg(2+) or 0.3 microM Nif reduced [Ca(2+)](cyt) and abolished plateau vasoconstriction. When added before PE, both Mg(2+) and Nif abolished the PE-evoked Ca(2+) oscillations and vasomotion. Mg(2+) dilated the PE-constricted arteries after a brief (< or =180-240 s) vasoconstriction, but Nif did not. Both agents also abolished the vasoconstriction attributed to Ca(2+) entry through store-operated channels (SOCs) during internal Ca(2+) store refilling that followed store depletion. The data suggest that Ca(2+) entry through SOCs helps maintain both myogenic tone and alpha(1)-adrenoceptor-induced tonic vasoconstriction.