Muscarinic Inhibition of L-type Ca^<2+> Channels in Guinea-Pig Tracheal Smooth Muscle Cells
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概要
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Modulation of L-type Ca^<2+> channels by acetylcholine (ACh) was studied in enzymatically isolated guinea-pig tracheal smooth muscle cells (TSMCs). ACh reversibly inhibited whole-cell L-type Ca^<2+> current measured with Ba^<2+> ions as charge carriers (I_<Ba>). With pipette solution containing 0.1mM EGTA, 1μM ACh induced transient inhibition of I_<Ba> followed by sustained inhigition (67.0±3.7% of the control, n=19). When intracellular Ca^<2+> concentration ([Ca^<2+>]_1) was fixed at 50nM by BAPTA-Ca^<2+> buffer in the pipette, the transient inhibition was abolished whereas the sustained inhibition (66.0±7.8%, n=6) still occurred, suggesting that the transient inhibition was attributed to inactivation of the channels induced by increase in [Ca^<2+>]_1. The sustained inhibition was abolished when [Ca^<2+>]_1 was fixed at zero. The sustained inhibition of I_<Ba> by 1μM ACh was observed in the presence of 10μM AF-DX 116, whereas it was not observed in the presence of 1μM 4-DAMP. ACh did not inhibit I_<Ba> in the presence of 1mM GDP-β-S in the pipette, whereas the drug irreversibly inhibited the current in the presence of 0.1mM GTP-γ-S in the pipette. Pretreatment of TSMCs with pertussis toxin did not altered the effects of ACh. Application of neither 1-oleoyl-2-acetyl-sn-glycerol (1μM) nor phorbol 12-myristate 13-acetate (1μM) reduced I_<Ba>. These results suggest that the sustained inhibition of I_<Ba> by ACh is mediated by Ca^<2+>-requiring and protein kinase C-independent mechanisms existing in the downstream of G-protein coupled with M_3 receptors.
- 日本平滑筋学会の論文
著者
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Kokubun Shinichiro
Department Of Physiology Nihon University School Of Medicine
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Kokubun Shinichiro
Departmen Of Physiology Nihon University School Of Medicine
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Yamashita Toshikazu
Department Of Physiology Nihon University School Of Medicine
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Yamashita Toshikazu
Departmen Of Physiology Nihon University School Of Medicine
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