Relationship of renal prostaglandins to three diuretics.
The effects of amiloride, a potassium-sparing diuretic, and of acetazolamide, a carbonic anhydrase inhibitor, were compared to those of triamterene, a potent prostaglandin stimulator which may result in acute renal failure after indomethacin pretreatment. Eighteen normal subjects on a constant sodium diet were given triamterene 200 mg/d, or amiloride 15 mg/d, or acetazolamide 750 mg/d for 3 days. Plasma potassium rose after triamterene and amiloride, and fell after acetazolamide. Natriuresis was increased after amiloride and acetazolamide, but not after triamterene. Plasma renin activity and urinary aldosterone were stimulated by the three diuretics. Triamterene induced a 4-fold increase in urinary prostaglandins E2 and F2 alpha and acetazolamide a 2-fold increase in prostaglandin E2 only, whereas amiloride showed no effect. No relationship was found between plasma or urinary electrolytes and urinary prostaglandins. Renal function was preserved in all cases. These results which show that amiloride, unlike triamterene, does not stimulate prostaglandins, suggest that nonsteroidal anti-inflammatory drugs (NSAID) which unmask triamterene nephrotoxicity may not constitute a hazard in association with amiloride. The prostaglandin response to acetazolamide may be indicative of adverse reactions during concomitant NSAID administration.
D000086:Acetazolamide / Q000494:pharmacology; D058186:Acute Kidney Injury / Q000139:chemically induced; D000328:Adult; D000584:Amiloride / Q000494:pharmacology; D000893:Anti-Inflammatory Agents / Q000009:adverse effects; D004232:Diuretics / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D011453:Prostaglandins / Q000096:biosynthesis* / Q000652:urine; D014223:Triamterene / Q000494:pharmacology
D000893:Anti-Inflammatory Agents; D004232:Diuretics; D011453:Prostaglandins; D000584:Amiloride; D000086:Acetazolamide; D014223:Triamterene