Günter Schultz

Lintschinger B

Rainer Strotmann

Silke Jung

Tim D. Plant

To investigate the possible role of members of the mammalian transient receptor potential (TRP) channel family (TRPC1–7) in vasoconstrictor-induced Ca2+entry in vascular smooth muscle cells, we studied [Arg8]-vasopressin (AVP)-activated channels in A7r5 aortic smooth muscle cells. AVP induced an increase in free cytosolic Ca2+concentration ([Ca2+]i) consisting of Ca2+release and Ca2+influx. Whole cell recordings revealed the activation of a nonselective cation current with a doubly rectifying current-voltage relation strikingly similar to those described for some heterologously expressed TRPC isoforms. The current was also stimulated by direct activation of G proteins as well as by activation of the phospholipase Cγ-coupled platelet-derived growth factor receptor. Currents were not activated by store depletion or increased [Ca2+]i. Application of 1-oleoyl-2-acetyl- sn-glycerol stimulated the current independently of protein kinase C, a characteristic property of the TRPC3/6/7 subfamily. Like TRPC6-mediated currents, cation currents in A7r5 cells were increased by flufenamate. Northern hybridization revealed mRNA coding for TRPC1 and TRPC6. We therefore suggest that TRPC6 is a molecular component of receptor-stimulated Ca2+-permeable cation channels in A7r5 smooth muscle cells.</jats:p

TRPC6 is a candidate channel involved in receptor-stimulated cation currents in A7r5 smooth muscle cells

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