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Rationale for Treatment of Heart Failure by Blockade of Ventricular Serotonin Receptors Appearing in Heart Failure

机译:通过封锁心力衰竭出现的心室血清素受体治疗心力衰竭的理由

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Serotonin (5-hydroxytryptamine, 5-HT) enhances contractility and causes arrhythmias through human atrial 5-HT4 receptors. We recently found that porcine and human as well as failing rat cardiac ventricle also responds to serotonin through 5-HT4 receptors which, like beta-adrenoceptors, are coupled via the G protein to increased cAMP formation1,2. In rats with 6-week post-infarction congestive heart failure (CHF), the maximal inotropic effect of serotonin was comparable in size with that of isoproterenol. Given the similar signalling systems utilised by the two receptors and that blockade of beta-adrenoceptors is beneficial in CHF, we propose that blockade of 5-HT4 receptors may also be beneficial in CHF.
机译:血清素(5-羟基 - 羟基胺,5-HT)增强了收缩性,并通过人体室间隔5-HT4受体引起心律失常。我们最近发现猪和人以及失败的大鼠心室还通过5-HT4受体响应血清素,与β-肾上腺素依有剂相同,通过G蛋白偶联至增加的阵营形成1,2。在6周后梗死后充血性心力衰竭(CHF)的大鼠中,血清素的最大官能效果与异丙肾上腺素的大小相当。鉴于两种受体使用的类似信号系统,并且β-肾上腺素受益剂在CHF中是有益的,我们提出阻断5-HT4受体也可能在CHF中有益。

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