Olsen M E, Hall J E, Montani J P, Cornell J E
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
J Hypertens Suppl. 1985 Dec;3(3):S255-8.
Previous studies suggest that the renal vasoconstrictor effect of angiotensin II (ANG II) is confined primarily to efferent arterioles, with little direct action on preglomerular vessels. The present study examined the role of prostaglandins (PG) in protecting preglomerular vessels from ANG II constriction. In dogs in which ANG II formation was blocked with captopril and renal artery pressure was servo-controlled, i.v. ANG II infusion (20 ng/kg per min) decreased renal blood flow (RBF) by about 50% while causing no significant change in glomerular filtration rate (GFR) and increasing filtration fraction (FF). After PG blockade, ANG II infusion decreased GFR by more than 30% and RBF by more than 50%, while causing much greater increases in calculated preglomerular resistance (RA) than in dogs without PG blockade. To prevent secondary changes in renal resistances via tubuloglomerular feedback (TGF), glomerular filtration was stopped by occluding the ureter during mannitol diuresis. After inhibition of TGF, ANG II decreased RBF markedly and increased glomerular hydrostatic pressure by 8-10 mmHg due to large increases in postglomerular resistance (RE) with no change in RA. After PG blockade and inhibition of TGF, ANG II decreased RBF by about the same amount as in control dogs but did not change glomerular hydrostatic pressure due to marked increases in both RA and RE. These data suggest that PGs selectively protect preglomerular vessels from ANG II constriction but do not interfere with the effect of ANG II on efferent arterioles.
以往的研究表明，血管紧张素II（ANG II）的肾血管收缩作用主要局限于出球小动脉，对肾小球前血管几乎没有直接作用。本研究探讨了前列腺素（PG）在保护肾小球前血管免受ANG II收缩影响方面的作用。在使用卡托普利阻断ANG II形成且肾动脉压力采用伺服控制的犬中，静脉输注ANG II（20 ng/kg每分钟）使肾血流量（RBF）降低约50%，而肾小球滤过率（GFR）无显著变化，滤过分数（FF）增加。PG阻断后，输注ANG II使GFR降低超过30%，RBF降低超过50%，同时与未进行PG阻断的犬相比，计算得出的肾小球前阻力（RA）升高幅度更大。为防止通过管球反馈（TGF）引起肾阻力的继发性变化，在甘露醇利尿期间通过阻断输尿管来停止肾小球滤过。抑制TGF后，ANG II使RBF显著降低，并使肾小球静水压升高8 - 10 mmHg，这是由于球后阻力（RE）大幅增加而RA无变化所致。PG阻断并抑制TGF后，ANG II使RBF降低的幅度与对照犬大致相同，但由于RA和RE均显著增加，肾小球静水压未发生变化。这些数据表明，PG可选择性地保护肾小球前血管免受ANG II的收缩作用，但不干扰ANG II对出球小动脉的作用。
