Beschreibung:
<jats:p>To investigate the possible role of members of the mammalian transient receptor potential (TRP) channel family (TRPC1–7) in vasoconstrictor-induced Ca<jats:sup>2+</jats:sup>entry in vascular smooth muscle cells, we studied [Arg<jats:sup>8</jats:sup>]-vasopressin (AVP)-activated channels in A7r5 aortic smooth muscle cells. AVP induced an increase in free cytosolic Ca<jats:sup>2+</jats:sup>concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) consisting of Ca<jats:sup>2+</jats:sup>release and Ca<jats:sup>2+</jats:sup>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 [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>. 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 Ca<jats:sup>2+</jats:sup>-permeable cation channels in A7r5 smooth muscle cells.</jats:p>