Toda N
Br J Pharmacol. 1984 Feb;81(2):301-7. doi: 10.1111/j.1476-5381.1984.tb10079.x.
In helical strips of dog renal and mesenteric arteries pre-contracted with prostaglandin F2 alpha (PGF2 alpha), endothelium-dependent relaxations were investigated. Removal of the endothelium was shown histologically by staining with silver nitrate and functionally by testing the inability of acetylcholine to induce arterial relaxations. When the endothelium was removed, relaxation of renal arteries to angiotensin (Ang) II was markedly suppressed, whereas relaxations induced by PGI2 or isoprenaline were attenuated only slightly. Removal of the endothelium attenuated the relaxant response of mesenteric arteries to histamine but did not significantly alter the response to PGI2. Treatment with indomethacin caused an additional attenuation of the relaxant response to histamine or a reversal of the Ang II-induced relaxation to a contraction in the arterial strips, from which the endothelium had been removed. Relaxation of renal arteries induced by Ang II and of mesenteric arteries induced by histamine is postulated to result from PGI2 released from the arterial wall. Therefore, it appears that the endothelium is a major site but not the only site responsible for drug-induced release of PGI2.
在预先用前列腺素F2α(PGF2α)预收缩的犬肾动脉和肠系膜动脉螺旋条上,研究了内皮依赖性舒张作用。通过硝酸银染色在组织学上显示内皮的去除,并通过测试乙酰胆碱不能诱导动脉舒张在功能上显示内皮的去除。当去除内皮时,肾动脉对血管紧张素(Ang)II的舒张作用明显受到抑制,而PGI2或异丙肾上腺素诱导的舒张作用仅略有减弱。去除内皮减弱了肠系膜动脉对组胺的舒张反应,但对PGI2的反应没有显著改变。用吲哚美辛处理导致对组胺的舒张反应进一步减弱,或在去除内皮的动脉条中使Ang II诱导的舒张反应逆转为收缩。推测Ang II诱导的肾动脉舒张和组胺诱导的肠系膜动脉舒张是由动脉壁释放的PGI2引起的。因此,似乎内皮是药物诱导的PGI2释放的主要部位,但不是唯一部位。