Schnermann J, Weber P C
Prostaglandins. 1982 Sep;24(3):351-61. doi: 10.1016/0090-6980(82)90162-9.
Experiments were performed in rats to study the effect of infusion of PGI2, PGE2, and PGF2 alpha on tubuloglomerular feedback responses (i.e. the change of SNGFR in response to a change of loop of Henle flow rate) in the presence and absence of simultaneous inhibition of endogenous PG synthesis with indomethacin. Infusion of PGI2 or PGE2 at rates that did not alter arterial blood pressure did not significantly modify the magnitude of feedback responses (PGI2 8.5 micrograms/hr, PGE2 85 micrograms/hr). Some inhibition of feedback responses was seen when PGI2 and PGE2 were administered at higher rates that were associated with a reduction of blood pressure (PGI2 20 micrograms/hr, PGE2 200 micrograms/hr). PGI2 (8.5 micrograms/hr) and PGE2 (85 micrograms/hr) largely prevented feedback inhibition induced by indomethacin. When given subsequent to indomethacin PGI2 and PGE2 restored feedback responsiveness almost to normal. In contrast, PGF2 alpha did not influence feedback inhibition caused by indomethacin. Infusion of PGI2 induced partial restoration of feedback responses in DOCA-salt treated animals in which the feedback system is virtually completely inactive. Our results indicate that availability of PGI2 or PGE2 is necessary for the normal operation of the tubuloglomerular feedback mechanism for control of nephron filtration rate.
在大鼠身上进行了实验，以研究在存在和不存在用吲哚美辛同时抑制内源性前列腺素合成的情况下，输注前列环素（PGI2）、前列腺素E2（PGE2）和前列腺素F2α（PGF2α）对肾小管-肾小球反馈反应（即单个肾单位肾小球滤过率（SNGFR）对髓袢流速变化的反应）的影响。以不改变动脉血压的速率输注PGI2或PGE2不会显著改变反馈反应的幅度（PGI2 8.5微克/小时，PGE2 85微克/小时）。当以与血压降低相关的较高速率给予PGI2和PGE2时，可观察到对反馈反应的一些抑制作用（PGI2 20微克/小时，PGE2 200微克/小时）。PGI2（8.5微克/小时）和PGE2（85微克/小时）在很大程度上阻止了吲哚美辛诱导的反馈抑制。在吲哚美辛之后给予PGI2和PGE2可使反馈反应性几乎恢复正常。相比之下，PGF2α不影响吲哚美辛引起的反馈抑制。输注PGI2可使去氧皮质酮-盐处理的动物（其反馈系统实际上完全无活性）的反馈反应部分恢复。我们的结果表明，PGI2或PGE2的可利用性对于控制肾单位滤过率的肾小管-肾小球反馈机制正常运作是必要的。
