Prevention of interstitial pressure change at unilateral nephrectomy by prostaglandin synthesis inhibition.

The mechanisms underlying the adaptive process in the remaining kidney after unilateral nephrectomy are not well known. In the present study adaptive changes in interstitial pressure conditions following uninephrectomy were investigated in male Sprague-Dawley rats. Direct subcapsular hydrostatic pressure recordings were made via microcatheters , renal lymph was collected for lymph flow rate estimations and determinations of lymph protein content and the urine flow rate and urinary excretion of sodium and potassium were measured, before and after contralateral nephrectomy. There was a significant rise in subcapsular hydrostatic pressure by about 50%, and in the lymph flow rate, by more than 100%, within 1 hr after nephrectomy. The protein concentration in collected renal lymph was significantly decreased (from 2.30 +/- 0.25 to 1.45 +/- 0.26 g/dl), compared with control collections in sham-operated animals (from 2.22 +/- 0.23 to 1.78 +/- 0.19 g/dl). These findings indicate an increased hydrostatic and decreased intersititial pressure in response to contralateral nephrectomy. Urine flow rate and electrolyte excretion were significantly elevated (urine flow rate by 92%, sodium excretion from 0.210 +/- 0.035 to 0.352 +/- 0.067 mumoles/min and potassium excretion from 0.306 +/- 0.074 to 1.617 +/- 0.228 mumoles/min). Inhibition of prostaglandin synthesis prior to nephrectomy abolished the lymph flow increase and oncotic pressure decrease and also the diuretic and natriuretic responses. The adaptively increased potassium excretion was, however, only blocked by diclofenac sodium and not by indomethacin. These results demonstrate the important role of the renal interstitium and the prostaglandin system in the renal adaptation to nephron loss.