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Corticotropin-releasing factor receptor-1: a therapeutic target for cardiac autonomic disturbances.

机译:促肾上腺皮质激素释放因子受体-1:心脏自主神经紊乱的治疗目标。

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摘要

Corticotropin-releasing factor (CRF), a neuropeptide involved in triggering a myriad of responses to fear and stress, is favourably positioned in the CNS to modulate the sympathetic and parasympathetic branches of the cardiac autonomic nervous system. In vivo studies suggest that central CRF inhibits vagal output and stimulates sympathetic activity. Therefore, CRF may function to inhibit exaggerated vagal activation that results in severe bradycardia or even vasovagal syncope. On the other hand, CRF receptor-1 (CRF(1)) antagonists increase cardiac vagal and decrease sympathetic activity, thereby also implicating CRF(1) as a therapeutic target for autonomic disturbances resulting in elevated sympathetic activity, such as hypertension and coronary heart disease. The central distribution of CRF(1) and the cardiovascular effects of CRF(1) agonists and antagonists, suggest it mediates CRF-induced autonomic changes. However, there is insufficient information regarding the autonomic effects of CRF(2)-selective compounds to rule out CRF(2) contribution. This review provides an update on the autonomic effects of CRF and the neuronal projections thought to mediate these cardiovascular responses.
机译:促肾上腺皮质激素释放因子(CRF)是一种参与触发对恐惧和压力的多种反应的神经肽,它位于CNS中以调节心脏自主神经系统的交感神经和副交感神经分支。体内研究表明,中央CRF抑制迷走神经输出并刺激交感神经活动。因此,CRF可能会抑制过度的迷走神经活化,从而导致严重的心动过缓甚至血管迷走性晕厥。另一方面,CRF受体1(CRF(1))拮抗剂会增加心脏迷走神经并降低交感神经活动,因此也暗示CRF(1)作为导致自主神经功能紊乱的治疗靶点,导致自主神经功能紊乱,导致交感神经活动增加,例如高血压和冠心病疾病。 CRF(1)的中央分布以及CRF(1)激动剂和拮抗剂的心血管作用表明它介导了CRF诱导的自主神经改变。但是,有关CRF(2)选择性化合物的自主作用的信息不足以排除CRF(2)的贡献。这篇评论提供了CRF的自主神经作用的最新进展以及认为介导这些心血管反应的神经元预测。

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