Mechanisms involved in serotonin-induced vasodilatation.

Blood vessels Pub Date : 1990-01-01 DOI:10.1159/000158802
E J Mylecharane
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引用次数: 33

Abstract

In vitro investigations have identified three major mechanisms which could contribute to the vasodilator action of serotonin (5-hydroxytryptamine, 5-HT): direct vascular smooth muscle relaxation; prejunctional inhibition of noradrenaline release from vascular sympathetic nerve terminals; and release of endothelium-derived relaxing factor (EDRF). In vivo studies have shown that in pig and cat common carotid circulations, rabbit hindquarter and mesenteric circulations, and rat systemic vasculature, direct vascular smooth muscle relaxation may be the predominant mechanism involved, but the contribution of EDRF release remains to be established. In other circulations in vivo (dog femoral and common carotid), prejunctional inhibition of vascular sympathetic tone is the predominant mechanism responsible for serotonin-induced vasodilatation. All of these actions are mediated by 5-HT1-like receptors, but different subtypes seem to be involved in each of these mechanisms. The prejunctional inhibitory receptor has been the most studied; depending on the tissue, these subtypes may resemble 5-HT1A, 5-HT1B, 5-HT1C or 5-HT1D binding sites, or the contractile receptor in dog saphenous vein.

5 -羟色胺诱导血管扩张的机制。
体外研究已经确定了血清素(5-羟色胺,5-HT)的血管扩张作用的三种主要机制:直接血管平滑肌松弛;血管交感神经末梢去甲肾上腺素释放的交界前抑制作用内皮源性松弛因子(EDRF)的释放。体内研究表明,在猪和猫的颈总动脉循环、兔的后躯和肠系膜循环以及大鼠的全身血管系统中,血管平滑肌的直接松弛可能是主要机制,但EDRF释放的贡献仍有待确定。在其他体内循环(犬股动脉和颈总动脉)中,交感神经张力的交界前抑制是5 -羟色胺诱导的血管舒张的主要机制。所有这些作用都是由5- ht1样受体介导的,但每种机制似乎都涉及不同的亚型。结膜前抑制受体被研究得最多;根据组织的不同,这些亚型可能类似于5-HT1A、5-HT1B、5-HT1C或5-HT1D结合位点,或犬隐静脉中的收缩受体。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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