Alon U, Davidai G, Harpaz S, Samenia N, Berant M, Better O S
Rambam Medical Center, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.
Miner Electrolyte Metab. 1988;14(6):338-42.
To clarify the possible role of renal prostaglandins (PGs) in the phenomenon of bile-induced diuresis in the dog, we studied the effect of in situ unilateral infusion of bile on kidney function and PGs excretion, before and after PG-synthetase inhibitor administration in anesthetized dogs. The contralateral intact kidney served as control. In the first group of 6 dogs, infusion of bile diluted 1:20 resulted in a significant increase in urinary flow (117%; p less than 0.05), sodium (61%; p less than 0.01), potassium (26%; p less than 0.05), PGE2 (240%; p less than 0.05) and PGF2 alpha (137%; p less than 0.05) excretion rates. Further significant increases in urinary flow, sodium and PGE2 excretion rates were noted with infusion of bile diluted 1:10. All parameters returned to basal levels upon cessation of bile infusion. Significant linear correlation coefficients (p less than 0.005) were found between PGE2 excretion rates and urinary flow (r = 0.72), sodium (r = 0.91) and potassium (r = 0.88) excretion rates. In a second group of 6 dogs, intravenous administration of PG-synthetase inhibitor abolished the increase in renal PGs excretion and the increments in the rates of urinary flow and solute excretion in response to bile infusion. These findings support the notion that the acute diuretic and natriuretic effect of bile, and presumably that of cholemia is mediated, in part, through stimulation of renal PGs synthesis.
