不同机制参与黄体酮扩张兔血管作用

用离体血管条灌流实验方法 ,观察黄体酮对血管条去甲肾上腺素 (NA) ,Ca Cl2 ,KCl反应的影响 ,并观察给予 L- NNA、甲烯蓝 (MB)、吲哚美辛、普萘洛尔及去除内皮细胞后 ,黄体酮扩张血管作用的变化 .结果发现 :黄体酮 10 -4 mol· L-1及 10 -5mol· L-1分别使 NA和无 Ca2 +高 K+Krebs液中 Ca Cl2 量效曲线明显右移 ,最大反应压低 ,PD2 ′分别为 3.51和 4 .56 .黄体酮 2 .5× 10 -4mol· L-1使无 Ca2 + 液中 NA10 -6mol· L-1收缩血管作用明显减弱 (p <0 .0 0 1) ,但不影响 Ca Cl210 mmol· L-1引起的收缩 .L - NNA,MB及去除内皮可明显减弱黄体酮扩张 KCl 4 0 mmol· L-1的收缩血管作用 ,但吲哚美辛和普萘洛尔无明显影响 .结果表明 :黄体酮可通过受体操纵 Ca2 + 通道抑制 IP3 途径引起的内 Ca2 + 释放 ,也可通过电压依赖式 Ca2 + 通道抑制外 Ca2 + 内流 ,使血管条舒张 ,其作用有内皮依赖性 ,部分与 NO和 c GMP有关

Different Mechanisms Mediated the Vasorelaxation Caused byProgesterone in Rabbits

The organ bath was used to observe the contractive response of aortic strip to noradrenaline (NA),CaCl 2, and KCl, and also observe the vasodilatory changes after administration L NNA, MB, indomethacin and propranolol respectively or denuded endothelium. The results were as follow: Progesterone caused the concentration response curves of NA in Krebs solution and CaCl 2in Ca 2+ free Krebs containing K+ to move right, and decreased the maximum responses. It also reduced the contractive response of NA in Ca 2+ free Krebs solution while it did not affect the contraction caused by CaCl 2. L NNA, MB or denuded endothelium remarkably decreased the dilatory effect of progesterone on aortic strip precontracted by KCl, but after administration indomethacin and propranolol its action had no obvious change. The results have indicated that progesterone can inhibit the Ca 2+ release by IP 3 pathway through ROC and also decrease Ca 2+ influx through PDC, and as a result lead to aortic relaxation which may be partly related to NO and cGMP as well.