Cardiovascular pharmacology of purines.

Cardiovascular pharmacology of purines.
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嘌呤的心血管药理学。

DOI:
10.1042/cs0920013
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发表时间:
1997
期刊:
影响因子:
6
通讯作者:
P. Smits
P. Smits
中科院分区:
医学2区
文献类型:
--
作者:
G. Rongen;J. Floras;J. Lenders;T. Thien;P. Smits

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1.本文综述了ATP和腺苷的细胞外作用,特别是它们在心血管调节中的作用。2. ATP作为交感神经系统内的共递质,也从内皮细胞和聚集的血小板释放。ATP作用于血管平滑肌细胞上的P2 x嘌呤受体以诱导血管收缩。刺激内皮细胞上的P2 γ嘌呤受体释放内皮源性舒张因子并引起血管舒张。ATP的这种双重作用可能具有病理生理学意义,可在内皮功能受损和血栓形成部位诱导血管痉挛。3.腺苷是由ATP的酶降解产生的。其形成在缺血期间增强。腺苷抑制去甲肾上腺素从交感神经末梢释放,通过内皮依赖性和内皮非依赖性作用引起血管舒张,具有重要的抗血管炎特性并预防缺血的有害后遗症。在人类中,腺苷引起由肾脏、心脏和前臂中的化学敏感受体和传入神经介导的交感神经兴奋反射。这种反射可能在运动和缺血期间活跃,由于其潜在的不良后果,在开发新疗法以增强人体内源性腺苷的抗缺血作用时应考虑这种反射。腺苷似乎介导缺血引起的疼痛;对腺苷敏感性降低可能是无症状缺血的基础。4.与腺苷形成或降解或与腺苷受体相互作用的新药正在开发中。这些在治疗局部缺血和其他循环障碍中具有潜在的治疗应用。
1. This review focuses on the extracellular actions of ATP and adenosine, and in particular their role in cardiovascular regulation. 2. ATP serves as a co-transmitter within the sympathetic nervous system, and is also released from endothelium and aggregating thrombocytes. ATP acts on P2x purinoceptors on vascular smooth muscle cells to induce vasoconstriction. Stimulation of P2y purinoceptors on endothelial cells releases endothelium-derived relaxing factors and causes vasodilatation. This dual action of ATP may have pathophysiological importance by inducing vasospasm at sites of impaired endothelial function and thrombus formation. 3. Adenosine is generated by enzymic degradation of ATP. Its formation is enhanced during ischaemia. Adenosine inhibits noradrenaline release from sympathetic nerve endings, causes vasodilatation via endothelium-dependent and endothelium-independent actions, has important anti-arrhythmic properties and prevents deleterious sequelae of ischaemia. In humans, adenosine evokes a sympatho-excitatory reflex mediated by chemically sensitive receptors and afferent nerves in the kidney, heart and forearm. This reflex may be active during exercise and ischaemia and, because of its potential adverse consequences, it should be considered when developing new therapies to potentiate the anti-ischaemic actions of endogenous adenosine in humans. Adenosine appears to mediate ischaemia-induced pain; a reduced sensitivity to adenosine may underlie silent ischaemia. 4. New drugs that interact with adenosine formation or degradation or with adenosine receptors are under development. These have potential therapeutic application in the treatment of ischaemia and other circulatory disorders.
DOI: 10.1073/pnas.89.16.7432
发表时间: 1992-08-15
影响因子: 11.1
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ZHOU, QY;LI, CY;CIVELLI, O
通讯作者: CIVELLI, O
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DOI: 10.1111/j.1749-6632.1989.tb22404.x
发表时间: 1989
影响因子: 5.2
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通讯作者: Ueno,M
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DOI: --
发表时间: 1993
期刊: The Journal of pharmacology and experimental therapeutics
影响因子: --
作者:
Amoah-Apraku,B;Xu,J;Lu,JY;Pelleg,A;Bruns,RF;Belardinelli,L
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DOI: 10.1161/01.cir.68.6.1254
发表时间: 1983-01-01
期刊: CIRCULATION
影响因子: 37.8
作者:
DIMARCO, JP;SELLERS, TD;BELARDINELLI, L
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DOI: 10.1152/ajpheart.1990.259.3.h820
发表时间: 1990-09-01
影响因子: --
作者:
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通讯作者: BROWN, AM