Minami Y, Toda N
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Arch Int Pharmacodyn Ther. 1988 May-Jun;293:186-95.
Helically cut strips of dog coronary and mesenteric arteries of proximal and distal portions contracted in response to angiotensin (ANG) II in a dose-dependent fashion. The contractions were greater in the distal portions than in the proximal portions. Mesenteric arteries responded to the peptide with a greater contraction than coronary arteries. The peptide-induced contraction was suppressed by treatment with saralasin and was potentiated by indomethacin; magnitudes of the potentiation were similar in coronary and mesenteric arteries and in proximal and distal portions. Concentrations of TRK-100, a stable analog of PGI2, equipotent to those of PGI2 released by ANG II, estimated from dose-response curves for TRK-100 and enhancement by indomethacin of ANG II-induced contractions, did not differ in proximal and distal portions. It appears that differences in the contractile response to ANG II depend on heterogeneity in ANG II receptors responsible for the arterial contraction, but not on differences in the PGI2 generation via ANG II receptor activation.
狗冠状动脉和肠系膜动脉近段和远段的螺旋形切割条带对血管紧张素（ANG）II呈剂量依赖性收缩反应。远段的收缩比近段更强烈。肠系膜动脉对该肽的收缩反应比冠状动脉更强。用沙拉新处理可抑制该肽诱导的收缩，而吲哚美辛可增强这种收缩；冠状动脉和肠系膜动脉以及近段和远段的增强幅度相似。根据TRK - 100的剂量反应曲线以及吲哚美辛对ANG II诱导收缩的增强作用估计，TRK - 100（一种PGI2的稳定类似物）与ANG II释放的PGI2等效的浓度在近段和远段并无差异。似乎对ANG II收缩反应的差异取决于负责动脉收缩的ANG II受体的异质性，而非通过ANG II受体激活产生PGI2的差异。
