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Am J Physiol Heart Circ Physiol 280: H2545-H2553, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 6, H2545-H2553, June 2001

Mechanisms of coronary artery depolarization by uridine triphosphate

Donald G. Welsh and Joseph E. Brayden

Department of Pharmacology, University of Vermont, Burlington, Vermont 05405

We sought to define the basic mechanisms by which pyrimidine nucleotides constrict rat coronary resistance arteries. Uridine triphosphate (UTP) caused a dose-dependent constriction in coronary arteries stripped of endothelium. UTP also depolarized and increased cytosolic Ca2+ in coronary smooth muscle cells. Nisoldipine, an antagonist of voltage-operated Ca2+ channels, blocked the rise in cytosolic Ca2+ and reduced UTP-induced vasoconstriction by ~75% which suggests a prominent role for depolarization in this constrictor response. The ionic basis of UTP-induced depolarization was subsequently explored in coronary smooth muscle cells using whole-cell patch-clamp electrophysiology. In the absence of K+ and with CsCl in the pipette, UTP (40 µM) activated a sustained inwardly rectifying current (-0.66 ± 0.10 pA/pF at -60 mV). A 100 mM reduction in bath Na+ shifted the reversal potential of this current (from -2 ± 1 to -28 ± 4 mV) and reduced the magnitude (from -2.26 ± 0.61 to -0.51 ± 0.11 pA/pF). In addition to activating a depolarizing cation current, UTP inhibited hyperpolarizing outward currents. Specifically, UTP inhibited ATP-sensitive and voltage-dependent K+ currents yet had no effect on inwardly rectifying and Ca2+-activated K+ channels. This study indicates that electromechanical coupling is integral to pyrimidine-induced constriction in coronary resistance arteries.

resistance; nonselective cation channels; potassium; smooth muscle; calcium


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