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Abstract
We examined the effects of pirmenol and disopyramide on the muscarinic acetylcholine receptor-operated K + current ( I K.ACh) in atrial cells and on experimental atrial fibrillation in isolated guinea-pig hearts. In isolated atrial myocytes, both pirmenol and disopyramide concentration dependently inhibited the I K.ACh induced by carbachol or intracellular loading of GTP γS. Their inhibitory effects on the carbachol-induced current were more potent than those on GTP γS-induced current, suggesting that these drugs inhibit I K.ACh mainly by blocking muscarinic receptors. In Langendorff-perfused hearts these drugs reversed the carbachol-induced decreases in effective refractory periods and atrial fibrillation threshold. These drugs may be useful for the prevention of vagally induced atrial fibrillation.
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