Treatment of functional GI disease: the complex pharmacology of serotonergic drugs. Reply from author

摘要: I thank Drs De Ponti & Crema [1] for their interest and valuable comments, which help to clarify some evolving concepts. would entirely agree that while cisapride can induce atrial tachycardia acting via cardiac 5-HT4 receptors, this is not the main cause of cardiotoxicity delayed repolarization muscle as shown by prolongation QT interval. As they have pointed out, several recent publications confirmed mechanism responsible likely be cisapride's action on human ether-a-go-go-related gene (HERG) product, rapidly activating delayed-rectifier K+ current in muscle. Mutations been associated with long [2] susceptibility induced arrthymias [3]. The HERG channel cavity lined aromatic residues, a feature distinguishes it from other channels. This appears render particularly susceptible drug interaction [4]. make very important point directly related receptor agonist properties, (tegaserod, mozapride) appear free effect [5]. I also like them correcting unintentional description buspirone 5-HT1p agonist. am further grateful drawing our attention work, suggests fundal relaxing sumatripan may mediated 5-HT1b/d receptors. encouraging since there are numerous agonists now development migraine market well value gastroenterologists.