Pugliese F, Ciabattoni G
Clin Exp Rheumatol. 1984 Oct-Dec;2(4):345-52.
This review examines the role of renal PGs in regulating glomerular function (RBF and GFR). The bulk of available evidence suggests that the glomerulus is the target structure for many vasoconstrictor agents, which stimulate renal synthesis of vasodilator PGs. PGE2 and PGI2 may regulate GFR and RBF by modulating either the vasoconstrictor actions on arterioles or the contractile activity of these agents on the glomerular mesangium. NSADs inhibit renal PG-synthesis at usual therapeutic dosage. In normal man these drugs appear not to affect GFR and RBF. In a number of renal ischemic states sustained by either exaggerated vasoconstrictor stimuli to the kidney or local reduction of vasodilator PGI2 synthesis, NSADs may exert deleterious effects on renal function. Selective sparing of renal cyclo-oxygenase activity of sulindac makes this drug safe in patients with severe cardiac, hepatic or glomerular disease.
