Okamura T, Minami Y, Toda N
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Pharmacology. 1989;38(5):279-88. doi: 10.1159/000138548.
In helical strips of monkey coronary and mesenteric arteries and dog mesenteric arteries partially contracted with prostaglandin (PG)F2 alpha, the mechanism of action of acetylcholine (ACh) has been analyzed by the use of pharmacological antagonists and by the endothelium-derived relaxing factor (EDRF) bioassay and the 6-keto PGF1 alpha radioimmunoassay. In conclusion, ACh releases vasodilator substance(s) from endothelium (EDRF) and also PGs from subendothelial tissues. Vasoconstrictor PGs appear to counteract the dilator action of EDRF in monkey coronary arteries, whereas vasodilator PG, possibly PGI2, appears to facilitate the relaxation caused by EDRF in monkey and dog mesenteric arteries.
在部分由前列腺素(PG)F2α引起收缩的猴冠状动脉和肠系膜动脉以及犬肠系膜动脉的螺旋条带中,已通过使用药理学拮抗剂、内皮衍生舒张因子(EDRF)生物测定法和6-酮-PGF1α放射免疫测定法分析了乙酰胆碱(ACh)的作用机制。总之,ACh从内皮释放血管舒张物质(EDRF),并且也从内皮下组织释放PG。血管收缩性PG似乎抵消了EDRF在猴冠状动脉中的舒张作用,而血管舒张性PG,可能是前列环素(PGI2),似乎促进了EDRF在猴和犬肠系膜动脉中引起的舒张。