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Acetylcholine (ACh) released from parasympathetic nerves binds to muscarinic (M2) ACh receptor (mAChR) in the heart, which leads to activation of muscarinic K(+) channel via the betagamma subunit of a G protein. The effect of a general anaesthetic (halothane) on the muscarinic K(+) channel (i(K,Ach)) in guinea-pig atrial cells was investigated using the whole-cell patch clamp technique. Halothane suppressed i(K,Ach), slowed down activation of i(K,Ach) and decreased peak i(K,Ach). When i(K,Ach) was activated by ACh acting via the muscarinic ACh receptors in the normal way, the decrease of i(K,Ach) was greater than the decrease when the muscarinic ACh receptor was bypassed and i(K,Ach) was activated by GTPgammaS. The above finding suggests that the suppression of i(K,Ach) by halothane is, in part, a result of the direct effect on the muscarinic K(+) channel or associated G protein. The decrease of i(K,Ach) by halothane may interfere with parasympathetic control of the heart.

Citation

W J Zang, X J Yu, Y M Zang. Effect of halothane on the muscarinic potassium current of the heart]. Sheng li xue bao : [Acta physiologica Sinica]. 2000 Apr;52(2):175-8

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PMID: 11961592

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