[Indomethacin and furosemide in patients with cardiac insufficiency. Kidney function, the renin-angiotensin system and renal prostaglandins].

Ten patients in heart failure of various etiologies underwent a placebo-controlled study to determine the effect of indomethacin (150 mg daily by mouth) on urine volume, sodium chloride excretion, glomerular filtration rate, renal prostaglandins, as well as plasma renin and aldosterone concentrations before and after administration of 40 mg frusemide by mouth. None had hyponatremia and plasma renin levels were within normal limits, but prostaglandin synthesis inhibition by indomethacin significantly reduced urine volume (-50%), sodium excretion (-70%) and glomerular filtration rate (-50%), as well as the urinary excretion of prostaglandin E2 (-80%) and 6-keto-prostaglandin F1 alpha (-70%). Frusemide-induced diuresis was halved by indomethacin. The suppression of renal prostaglandin excretion induced by inhibition of cyclooxygenase was not much influenced by frusemide. Plasma renin and aldosterone concentrations after indomethacin administration were not significantly raised by frusemide. The results indicate that renal prostaglandin synthesis is of great importance in the pathophysiology and treatment of mild to moderate heart failure.