Molleman A, Liu L W, Huizinga J D
Department of Medicine, McMaster University, Hamilton, ON, Canada.
Can J Physiol Pharmacol. 2001 Jan;79(1):34-42.
Muscarinic receptor mediated membrane currents and contractions were studied in isolated canine colon circular smooth muscle cells. Carbachol (10(-5) M) evoked a slow transient inward current that was superimposed by a transient outward current at holding potentials greater than -50 mV. Carbachol contracted the cells by 70 +/- 2%. The effects of carbachol were blocked by atropine (10(-6) M), tetraethyl ammonium (20 mM), and BAPTA-AM (25 mM applied for 20 min). The inward current and contraction were not sensitive to diltiazem (10(-5) M), nitrendipine (3 x 10(-7) M), niflumic acid (10(-5) M), or N-phenylanthranilic acid (10(-4) M), but were gradually inhibited after repetitive stimulations in Ca2+ free solution. Ni2+ (2 mM) inhibited the inward current by 67 +/- 4%. The inward current reversed at +15 mV. The outward component could be selectively inhibited by iberiotoxin (20 nM) or by intracellular Cs+. Repeated stimulation in the presence of cyclopiazonic acid (CPA, 3 microM) inhibited the carbachol-induced outward current and partially inhibited contraction. CPA did not inhibit the inward current. In conclusion, muscarinic receptor stimulation evoked a CPA-sensitive calcium release that caused contraction and a CPA-insensitive transient inward current was activated that is primarily carried by Ca2+ ions and is sensitive to Ni2+.
在分离的犬结肠环形平滑肌细胞中研究了毒蕈碱受体介导的膜电流和收缩。卡巴胆碱（10⁻⁵ M）诱发了一种缓慢的瞬时内向电流，在大于 -50 mV 的钳制电位下叠加有瞬时外向电流。卡巴胆碱使细胞收缩了 70±2%。卡巴胆碱的作用被阿托品（10⁻⁶ M）、四乙铵（20 mM）和 BAPTA-AM（25 mM 作用 20 分钟）阻断。内向电流和收缩对地尔硫䓬（10⁻⁵ M）、尼群地平（3×10⁻⁷ M）、氟尼酸（10⁻⁵ M）或 N-苯基邻氨基苯甲酸（10⁻⁴ M）不敏感，但在无钙溶液中重复刺激后逐渐受到抑制。Ni²⁺（2 mM）使内向电流抑制了 67±4%。内向电流在 +15 mV 处反转。外向成分可被iberiotoxin（20 nM）或细胞内 Cs⁺选择性抑制。在环匹阿尼酸（CPA，3 μM）存在下重复刺激可抑制卡巴胆碱诱导的外向电流并部分抑制收缩。CPA 不抑制内向电流。总之，毒蕈碱受体刺激诱发了一种对 CPA 敏感的钙释放，导致收缩，并激活了一种对 CPA 不敏感的瞬时内向电流，该电流主要由 Ca²⁺离子携带且对 Ni²⁺敏感。
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