Persson A E, Hahne B, Selén G
Can J Physiol Pharmacol. 1983 Nov;61(11):1317-23. doi: 10.1139/y83-190.
The prostaglandins (PG) of the renal medulla might affect the nephron and the cortical arteriolar function via the tubular route. To investigate this question PGE2 (1 microgram/mL), PGF2 alpha (10 micrograms/mL), or PGI2 (1 ng/mL) was added to the tubular perfusion solution when the characteristics of the tubuloglomerular feedback (TGF) control were measured. The experiments were performed on Sprague-Dawley rats. The proximal tubular stop-flow pressure (PSF) was measured upstream to a wax block, while at the same time the distal nephron was perfused with prostaglandin-containing or prostaglandin-free solutions at different flow rates varying from 0 to 50 nL/min. The maximal drop in PSF (delta PSF) and the tubular flow rate at which 50% of the delta PSF response was obtained, the turning point (TP), were determined. When PGE2 or PGF2 alpha was added to the tubular perfusion solution in the control animals a significant increase in feedback sensitivity was found. After 10 min of tubular PGI2 perfusion the feedback sensitivity was almost completely abolished, with a delta PSF of 0.8 mmHg (1 mmHg = 133.322 Pa) (control 8.4 mmHg) and a TP of greater than 40 nL/min (control 22 nL/min). After nephrectomy the feedback sensitivity was reduced, with a delta PSF of 2.0 mmHg and a TP of greater than 40 nL/min. When PGE2 was added to the tubular perfusion solution in the uninephrectomized animals, the feedback sensitivity was increased to the control level, with a delta PSF of 8.2 mmHg and a TP of 20.0 nL/min.(ABSTRACT TRUNCATED AT 250 WORDS)