Abstract:
:We studied the contribution of store-operated or capacitative Ca2+-entry (SOCE or CCE, respectively) through store-operated Ca2+ channels (SOCCs) and the contribution of Ca2+-entry through receptor-operated, non-selective cation channels (ROCCs or NSCCs, respectively), on the M3-receptor-mediated (270 nM Ach) contractile response of porcine coronary smooth muscle strips by means of the respective inhibitors. In the presence of L-VOCC blockade (1 microM verapamil), LOE 908 (inhibition of NSCCs) decreased the contractile response to 75+/-5% (p<0.01, n=6), 2-APB (inhibition of SOCCs) and SK and F 96365 (inhibition of SOCCs and of NSCCs) decreased the response to 45+/-4% (p<0.001, n=10) and to 23+/-2% (p<0.001, n=5), respectively (control: Ach response in the presence of verapamil alone). In the absence of L-VOCC blockade, LOE 908 reduced the Ach-response to 49+/-7% (p<0.001, n=8) and SK and F 96365 to 3+/-2% (p<0.001, n=4) of control, whereas 2-APB transiently increased the response (peak effect: 130+/-11%; p<0.05, n=8). We conclude: (1) the main source of activator Ca2+ during the M3-receptor-mediated contractile response is the Ca2+ influx through L-VOCCs; (2) however, in the presence of L-VOCC blockade, the contractile response is mainly due to Ca2+-entry through SOCCs; (3) NSCCs may be considerably involved in M3-receptor-mediated contraction as they may serve to depolarize the membrane potential and, thus, to open L-VOCCs; (4) in primary tissue of vascular smooth muscle, both, SOCE and Ca2+-entry through NSCCs are activated during M3-receptor stimulation.
journal_name
Cell Calciumjournal_title
Cell calciumauthors
Weirich J,Dumont L,Fleckenstein-Grün Gdoi
10.1016/j.ceca.2005.06.035keywords:
subject
Has Abstractpub_date
2005-11-01 00:00:00pages
457-67issue
5eissn
0143-4160issn
1532-1991pii
S0143-4160(05)00123-5journal_volume
38pub_type
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