Wilson W R, Greenberg S, Kadowitz P J, Diecke F P, Long J P
J Pharmacol Exp Ther. 1975 Dec;195(3):567-76.
The effects of prostaglandin A2 (PGA2) and prostaglandin B2 (PGB2) on vascular smooth muscle tone, electrolyte movements and responses to vasoactive stimuli were evaluated with superfused canine tibial arteries. PGA2 and PGB2 constricted superfused tibial arteries. PGB2 was 10.7 (8.3-14.1) times more potent as a constrictor than PGA2. PGA2 and PGB2-induced vasoconstriction was associated with a decrease in 22Na efflux and a tendency toward an increase in cellular sodium (expressed as micromoles per gram of wet weight). These prostaglandins also decreased the total potassium content of tibial arteries. 45Ca exchange was enhanced by PGA2 and PGB2. The time course of PG-induced increases in 45Ca efflux was similar to the temporal increase in force produced by PGA2 and PGB2. The duration of the contractile response to barium chloride was greatly prolonged during superfusion with both PGA2 and PGB2. These effects were probably not mediated by PG-induced alterations in the resting membrane potential of tibial arteries since presumed depolarization by both high potassium and zero-potassium physiologic saline solutions did not mimic the effects of these prostaglandins on vascular smooth muscle tone or responses to barium chloride. These data suggest that PGA2 and PGB2 may increase tone of vascular smooth muscle by inhibition of those processes involved in sequestration of calcium ion, i.e., the relaxation process, rather than acting on the contractile process.
利用灌注的犬胫骨动脉，评估了前列腺素A2（PGA2）和前列腺素B2（PGB2）对血管平滑肌张力、电解质转运以及对血管活性刺激反应的影响。PGA2和PGB2使灌注的胫骨动脉收缩。PGB2作为收缩剂的效力比PGA2强10.7（8.3 - 14.1）倍。PGA2和PGB2诱导的血管收缩与22Na外流减少以及细胞内钠含量增加的趋势相关（以每克湿重微摩尔数表示）。这些前列腺素还降低了胫骨动脉的总钾含量。PGA2和PGB2增强了45Ca交换。PG诱导的45Ca外流增加的时间进程与PGA2和PGB2产生的张力随时间增加相似。在同时用PGA2和PGB2灌注期间，对氯化钡的收缩反应持续时间大大延长。这些作用可能不是由PG诱导的胫骨动脉静息膜电位改变介导的，因为高钾和零钾生理盐溶液假定的去极化并未模拟这些前列腺素对血管平滑肌张力或对氯化钡反应的作用。这些数据表明，PGA2和PGB2可能通过抑制参与钙离子螯合的过程，即舒张过程，而不是作用于收缩过程来增加血管平滑肌张力。
