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Am J Physiol Heart Circ Physiol (August 15, 2002). doi:10.1152/ajpheart.00260.2002
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Articles in PresS, published online ahead of print August 15, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00260.2002
Submitted on March 25, 2002
Accepted on August 9, 2002

Mg2+ Blocks Myogenic Tone, but not K+ -induced Constriction: Role for Store-operated Channels in Small Arteries

Jin Zhang1, Withrow G Wier1, and Mordecai P Blaustein1*

1 Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA

* To whom correspondence should be addressed. E-mail: mblauste{at}umaryland.edu.

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-4AM 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. Subsequent addition of 10 mM Mg2+ or 0.3 µM Nif reduced [Ca2+]CYT and abolished the plateau vasoconstriction. When added before PE, both Mg2+ and Nif abolished the PE-evoked Ca2+ oscillations and vasomotion, and Mg2+ dilated the PE-constricted arteries after a brief (<=180-240 sec) 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.




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