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Institut für Pharmakologie, Freie Universität Berlin, 14195 Berlin, Germany
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 C
-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.
transient receptor potential channel; calcium ion influx; receptor-operated channel
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