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1 Pharmacology, Colleg of Medicine, University of Vermont, Burlington, Vermont, USA
* To whom correspondence should be addressed. E-mail: sreading{at}uvm.edu.
We tested the hypothesis that TRPC3, a member of the canonical transient receptor potential (TRPC) family of channels, mediates agonist-induced depolarization of arterial smooth muscle cells. In support of this hypothesis, we observed that suppression of arterial smooth muscle cell (SMC) TRPC3 expression using antisense oligodeoxynucleotides significantly decreased the depolarization and constriction of intact cerebral arteries in response to uridine triphosphate (UTP). In contrast, depolarization and contraction of SMC's induced by increased intravascular pressure, i.e. myogenic responses, were not altered by TRPC3 suppression. Interestingly, UTP-evoked responses were not affected by suppression of a related TRP channel, TRPC6, which was previously found to be involved in myogenic depolarization and vasoconstriction. In patch clamp experiments, UTP activated a whole cell current that was greatly reduced or absent in TRPC3 antisense-treated SMC's. These results indicate that TRPC3 mediates UTP-induced depolarization of arterial SMC's and that TRPC3 and TRPC6 may be differentially regulated by receptor activation and mechanical stimulation, respectively.
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