The renal response to ureteral obstruction.
The renal pathophysiology during ureteral obstruction was investigated in rat experiments, especially designed to study the role of the tubuloglomerular feedback (TGF) control mechanism. This mechanism, operating by sensing the distal delivery of fluid to the macula densa site, regulates the glomerular capillary pressure (PGC) and the glomerular filtration rate (GFR). Interstitial pressure conditions are known to influence the sensitivity of this control mechanism. Micropuncture experiments were performed to investigate the TGF activity before, during and after release of 2 h unilateral ureteral obstruction (UUO) and after 24 h UUO and bilateral ureteral obstruction (BUO). Renal interstitial hydrostatic and oncotic pressure, proximal stop-flow pressure (PSF) and GFR were also determined. In other experiments, the effects of indomethacin on renal pelvic pressure and PGC, estimated from PSF, were studied during the initial vasodilatory phase of UUO. Cortical and regional medullary blood flow was measured using a combination of labelled microspheres and the 86-Rb extraction method. The present results indicate that the initial vasodilatation, demonstrated by an increased PGC and accompanied by an elevated renal pelvic pressure, was caused by prostaglandin release. These pressures could be reduced by injection of indomethacin. Blood flow measurements revealed that the initial vasodilatation seems to occur both in the cortex and in the medulla, but after a few hours progressive vasoconstriction took place in all regions of the kidney. Two hours of UUO caused increased interstitial hydrostatic and decreased oncotic pressure and the TGF response was abolished. This phenomenon participated in the vasodilatory process at this stage of UUO. After release of 2 h UUO, GFR was reduced, indicating vasoconstriction, probably caused by activation of the highly sensitized TGF control mechanism seen in this situation. At 24 h of UUO there was a normal hydrostatic and high oncotic pressure and high TGF sensitivity. These findings contrast to those at 24 h of BUO, with normal interstitial pressure conditions and a slight decrease in TGF sensitivity. These differences between animals with UUO and BUO might be of importance for the absence of post-obstructive diuresis in UUO and the presence of this phenomenon in BUO animals.
D000818:Animals; D005246:Feedback; D005260:Female; D005919:Glomerular Filtration Rate; D006874:Hydrostatic Pressure; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000098:blood supply; D007684:Kidney Tubules / Q000503:physiopathology; D008297:Male; D011312:Pressure; D051381:Rats; D011919:Rats, Inbred Strains; D012079:Renal Circulation; D014517:Ureteral Obstruction / Q000503:physiopathology*; D014664:Vasodilation
D007213:Indomethacin