Spokas E G, Folco G C
Eur J Pharmacol. 1984 Apr 20;100(2):211-7. doi: 10.1016/0014-2999(84)90225-5.
We examined the endothelial dependence of responses to ACh and some vasodilator drugs by using the central tail artery of the rat perfused with Krebs buffer. Perfusion with ACh (100 nM-100 microM) produced dose-dependent vasodilatation of arteries preconstricted with norepinephrine and antagonized pressor responses to periarterial electrical stimulation. Endothelium was removed by introducing a fine catheter through the lumen or a stream of gas (O2 95%-CO2 5%) intraluminally. Both procedures prevented the vasodilator effect of ACh. Gassing also abolished the vasodilatation in response to hydralazine 334 nM but not to equidilator amounts of papaverine 13 microM, or nitroglycerin 50 nM. These results indicating endothelial dependence of hydralazine and ACh responses are in accord with our previous studies on vascular rings.
我们通过使用用 Krebs 缓冲液灌注的大鼠尾中央动脉,研究了对乙酰胆碱(ACh)和一些血管舒张药物反应的内皮依赖性。用 ACh(100 nM - 100 μM)灌注可使预先用去甲肾上腺素收缩的动脉产生剂量依赖性血管舒张,并拮抗对动脉周围电刺激的升压反应。通过经管腔插入细导管或腔内注入气流(95% O₂ - 5% CO₂)去除内皮。这两种方法均能阻止 ACh 的血管舒张作用。通气还消除了对 334 nM 肼屈嗪的血管舒张反应,但对等量的 13 μM 罂粟碱或 50 nM 硝酸甘油的血管舒张反应无影响。这些表明肼屈嗪和 ACh 反应具有内皮依赖性的结果与我们之前对血管环的研究一致。