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内皮依赖性抑制利用细胞外钙来实现动脉对血管收缩剂的反应。

Endothelium-dependent inhibition of the use of extracellular calcium for the arterial response to vasoconstrictor agents.

作者信息

Oshiro M E, Paiva A C, Paiva T B

出版信息

Gen Pharmacol. 1985;16(6):567-72. doi: 10.1016/0306-3623(85)90144-2.

Abstract

The responses of rabbit mesenteric or coeliac artery rings to angiotensin II or adrenaline (but not to K+) were enhanced by endothelium destruction (by rubbing). Potentiation by indomethacin of the response to the agonists was observed in rubbed rings but not in intact ones. Both angiotensin II and adrenaline (in the presence of propranolol and prazosin) induced endothelium-dependent relaxation of the arteries. Rubbed rings, but not intact ones, contracted when Ca2+ was added to a previously Ca2+-free medium containing angiotensin II or adrenaline. The vasoconstrictor response appears to be modulated by the regulation of receptor-operated Ca2+ channels through EDRF released by the endothelium and by some cyclo-oxygenase product at the level of the smooth muscle cell membrane.

摘要

兔肠系膜或腹腔动脉环对血管紧张素II或肾上腺素(而非钾离子)的反应,经内皮破坏(通过摩擦)后增强。在摩擦过的动脉环中观察到吲哚美辛对激动剂反应的增强作用,而在完整动脉环中未观察到。血管紧张素II和肾上腺素(在普萘洛尔和哌唑嗪存在的情况下)均可诱导动脉的内皮依赖性舒张。当向先前不含钙离子且含有血管紧张素II或肾上腺素的培养基中添加钙离子时,摩擦过的动脉环会收缩,而完整动脉环则不会。血管收缩反应似乎是通过内皮释放的内皮舒张因子(EDRF)以及平滑肌细胞膜水平上的某些环氧化酶产物对受体操纵性钙离子通道的调节来调控的。

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