Pace-Asciak C R, Rosenthal A
Prostaglandins. 1981 Oct;22(4):567-74. doi: 10.1016/0090-6980(81)90066-6.
PGE2 can vasoconstrict or vasodilate the isolated Krebs-perfused rat kidney depending on the tone of the renal vasculature. Thus, it is weakly constrictor (thres-hold 5-10 ng bolus dose) in the perfused kidney whose perfusion pressure is 47 +/- 2 SD mmHg (n = 6), but becomes a vasodilator (threshold approximately 10 pg) in the kidney whose perfusion pressure has been raised to 73 +/- 6 SD mmHg (n = 6) or 121 +/- 8 SD mmHg (n = 6) through constant infusion of Vasopressin (0.1 and 0.25 mU/ml respectively. PGE1 was equally effective as PGE2 while other PGs, I2, I1, and 6-keto E1, were less effective in opposing vasoconstriction. PGF2 alpha was inactive up to a dose of 10 ng.
根据肾血管的紧张度，前列腺素E2（PGE2）可使离体的用Krebs液灌注的大鼠肾脏血管收缩或舒张。因此，在灌注压为47±2标准差毫米汞柱（n = 6）的灌注肾脏中，它是弱收缩剂（推注剂量阈值为5 - 10纳克），但在通过持续输注血管加压素（分别为0.1和0.25毫单位/毫升）使灌注压升高到73±6标准差毫米汞柱（n = 6）或121±8标准差毫米汞柱（n = 6）的肾脏中，它则成为血管舒张剂（阈值约为10皮克）。前列腺素E1（PGE1）与PGE2的效果相同，而其他前列腺素，如前列环素（I2）、前列异环素（I1）和6 - 酮 - 前列腺素E1（6 - keto E1），在对抗血管收缩方面效果较差。前列腺素F2α（PGF2α）在剂量高达10纳克时无活性。
