Renal function and urinary prostanoid excretions in salt-depleted women: comparative effects of enalapril and indomethacin treatments

The acute effects on urinary prostanoid excretion and on renal function ind uced by pharmacological inhibition of either the angiotensin-converting enz yme or of the cyclooxygenase system, respectively, have been studied in hea lthy salt-depleted women. Two experimental groups were studied during salt depletion, SD1 (n=8) and natriuretic and potassium sparing treatment. Paire d studies were performed in the absence and in the presence of enalapril (S D1 group) or indomethacin (SD2 group). In both paired studies renal functio n was estimated by the clearance (cl.) method and the urinary concentration s of PGE(2), 6-keto-PGF(1 alpha) and TXB2 were estimated by RIA during sust ained hypotonic polyuria (induced by oral water load). Enalapril did not in fluence urinary excretion of prostanoids. Its main significant effects were : (a) a reduction in mean arterial pressure (MAP); (b) an increase ion free -water cl. (C-H2O) and a reduction in osmolar cl. (C-osm); (c) a reduction in the absolute and fractional urinary excretions of sodium and chloride; a nd (d) a reduction in both the plasma concentration and urinary excretion o f potassium. The urinary flow rate and the creatinine cl. were not signific antly affected. Indomethacin reduced urinary excretion of prostanoids and i n addition it produced the following significant effects: (a) a reduction i n urinary flow rate, C-H2O and C-osm values, and in absolute and fractional urinary excretions of sodium and chloride; and (b) an increase in plasma p otassium concentration. MAP, creatinine cl. and urinary potassium excretion were not significantly affected. With regard to the main parameters, both enalapril and indomethacin exerted similar effects on urinary sodium and ch loride excretion but opposite effects on C-H2O and plasma potassium concent ration. In conclusion, after enalapril in a salt-depleted state, the functional exp ression of acute angiotensin II deprivation was partially masked by the act ivation of a homeostatic system responsible both for improvement in renal s alt conservation and for facilitated cellular potassium uptake. After indom ethacin in the same setting, the results were consistent with a differentia l role of prostanoids in modulating or mediating the activities of neuro-ho rmonal agonists.