McQueen D, Bell K
Eur J Pharmacol. 1976 Jun;37(2):223-35. doi: 10.1016/0014-2999(76)90029-7.
Conflicting evidence exists regarding the ability of PGE1 to normalize blood pressure in renal hypertensive rats. We performed experiments to determine the effect of PGE1 (15 mug/kg i.p. daily for 3 weeks) in renal hypertensive Wistars and found no significant change in systolic pressure. A higher dose (150 mug/kg i.p.) lowered pressure after 14 days of treatment, but not back to control levels. Further investigations are required to establish the mechanism whereby PGE1 evokes this fall. To test the hypothesis that endogenous prostaglandins have a hypotensive function in renal hypertension, experiments were performed using sodium meclofenamate to inhibit prostaglandin biosynthesis. In chronic hypertensive rats the drug had no significant effect, while in the acute phase of renal hypertension there was a dose-dependent inhibition of the pressure rise. The possibility is suggested that prostaglandins may initiate or sustain the acute phase of renal hypertension in rats.
关于前列腺素E1(PGE1)使肾性高血压大鼠血压恢复正常的能力,存在相互矛盾的证据。我们进行了实验,以确定PGE1(每天腹腔注射15微克/千克,持续3周)对肾性高血压Wistar大鼠的影响,结果发现收缩压没有显著变化。更高剂量(150微克/千克腹腔注射)在治疗14天后降低了血压,但未降至对照水平。需要进一步研究以确定PGE1引起这种血压下降的机制。为了检验内源性前列腺素在肾性高血压中具有降压功能的假设,使用甲氯芬那酸钠抑制前列腺素生物合成进行了实验。在慢性高血压大鼠中,该药物没有显著作用,而在肾性高血压急性期,存在剂量依赖性的血压上升抑制作用。这表明前列腺素可能引发或维持大鼠肾性高血压的急性期。