Schor N, Brenner B M
Hypertension. 1981 Nov-Dec;3(6 Pt 2):II-81-5. doi: 10.1161/01.hyp.3.6_pt_2.ii-81.
We studied the role of the renin-angiotensin system in the vasoconstrictor effect induced by prostaglandins (PG) on the renal microcirculation in 25 euvolemic Munich-Wistar rats. Infusions of subvasodepressor doses of PgE2 and PGI2 led to lower mean values for single nephron (SN) glomerular filtration rate (GFR), total kidney GFR, glomerular plasma flow rate, QA, and ultrafiltration coefficient (Kf) than were found in animals given vehicle alone (control group). On the other hand, the mean values for glomerular transcapillary hydraulic pressure difference, delta P, and total renal arteriolar resistance, RTA, tended to be higher in the experimental groups. The effects of PGI2 on the renal microcirculation were more pronounced than for PGE2. These increases in delta P and RTA and decreases in QA and Kf are typical of changes induced by angiotensin II (AII). To further explore this AII-like phenomenon, an infusion of saralasin, a competitive AII antagonist, was used. Indeed, when saralasin was infused together with either PGE 2 or PGI2 the previously noted effects on delta P, QA, RTA and Kf were largely abolished. Thus, saralasin transformed the renal action of PGE2 and PGI2 from vasoconstrictor (low QA, high RTA) to vasodilator (high QA and low RTA). Therefore, the effects of nonvasodepressor doses of PGE2 and PGI2 on the renal microcirculation appear to depend on an intermediate action of AII.
我们研究了肾素 - 血管紧张素系统在25只血容量正常的慕尼黑 - 威斯塔大鼠肾微循环中前列腺素（PG）诱导的血管收缩效应中的作用。输注低于血管舒张降压剂量的前列腺素E2（PgE2）和前列环素（PGI2）导致单肾单位（SN）肾小球滤过率（GFR）、总肾GFR、肾小球血浆流速、QA和超滤系数（Kf）的平均值低于仅给予赋形剂的动物（对照组）。另一方面，实验组中肾小球跨毛细血管液压差（delta P）和总肾小动脉阻力（RTA）的平均值往往更高。PGI2对肾微循环的影响比PGE2更明显。delta P和RTA的增加以及QA和Kf的降低是血管紧张素II（AII）诱导变化的典型特征。为了进一步探究这种类似AII的现象，使用了竞争性AII拮抗剂沙拉新进行输注。事实上，当沙拉新与PGE2或PGI2一起输注时，先前观察到的对delta P、QA、RTA和Kf的影响在很大程度上被消除。因此，沙拉新将PGE2和PGI2的肾脏作用从血管收缩剂（低QA，高RTA）转变为血管舒张剂（高QA和低RTA）。因此，非血管舒张降压剂量的PGE2和PGI2对肾微循环的影响似乎取决于AII的中间作用。
