Suppr超能文献

猫肠系膜和后肢血管床对ATPγS的不同反应。

Differential responses to ATPgammaS in the mesenteric and hindlimb vascular bed of the cat.

作者信息

Shah M K, Champion H C, Bivalacqua T J, Kadowitz P J

机构信息

Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.

出版信息

Life Sci. 2001 Oct 12;69(21):2561-71. doi: 10.1016/s0024-3205(01)01336-4.

Abstract

The mechanism by which the purinergic agonist adenosine 5'-O-(3 thiotriphosphate) (ATPgammaS) decreases vascular resistance was investigated in the mesenteric and hindlimb vascular beds of the cat. Injections of ATPgammaS into the hindlimb perfusion circuit elicited dose-dependent decreases in perfusion pressure while injections into the mesenteric circuit produced a biphasic response with an initial vasopressor response followed by a vasodepressor response. In the mesenteric vascular bed the pressor response to ATPgammaS was blocked by a P2X1 receptor antagonist. Also an inhibitor of nitric oxide synthase enhanced the vasoconstrictive responses to ATPgammaS. However, the vasodepressor response in the mesenteric bed was not altered by the adminstration of an alpha adrenergic receptor antagonist, a cyclooxygenase inhibitor, a P2Y1 receptor antagonist, or a K+ATP channel blocking agent. These data suggest that the vasopressor response to ATPgammaS in the mesenteric vascular bed of the cat is mediated via P2X1 receptor activation. The differential responses to ATPgammaS in the hindlimb and mesentery suggest differences in purinergic receptor distribution in the vascular system of the cat. In addition, the results suggest that prostaglandin synthesis, P2Y1 receptor activation, alpha receptor inhibition, and K+ATP channels activation play little to no role in mediating the vascular response to ATPgammaS in the mesentery of the cat.

摘要

在猫的肠系膜和后肢血管床中,研究了嘌呤能激动剂5'-O-(3-硫代三磷酸)腺苷(ATPγS)降低血管阻力的机制。将ATPγS注入后肢灌注回路会引起灌注压呈剂量依赖性降低,而注入肠系膜回路则产生双相反应,先是初始的升压反应,随后是降压反应。在肠系膜血管床中,对ATPγS的升压反应可被P2X1受体拮抗剂阻断。此外,一氧化氮合酶抑制剂可增强对ATPγS的血管收缩反应。然而,肠系膜床中的降压反应不会因给予α肾上腺素能受体拮抗剂、环氧化酶抑制剂、P2Y1受体拮抗剂或K⁺ATP通道阻断剂而改变。这些数据表明,猫肠系膜血管床中对ATPγS的升压反应是通过P2X1受体激活介导的。后肢和肠系膜对ATPγS的不同反应表明猫血管系统中嘌呤能受体分布存在差异。此外,结果表明前列腺素合成、P2Y1受体激活、α受体抑制和K⁺ATP通道激活在介导猫肠系膜对ATPγS的血管反应中几乎不起作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验