Acetylsalicylic acid, administered intravenously in a dose of 120 mg+250 mg/h, markedly decreased the urinary excretion of sodium and chloride, and slightly depressed potassium excretion, so that the ratio of urinary concentrations of potassium to sodium increased after ASA. Osmolar and free water clearances also diminished during water diuresis, and free water reabsorption (TcH2O) decreased after ASA during mannitol diuresis. Glomerular filtration rate and urine flow rate changed little. When infused directly into a renal artery, ASA exhibited identical action on both kidneys, indicating that the renotropic action is mediated by some endogenous humoral agents or by some metabolites of ASA. A dose of 100 mg i.v. of spironolactone, a aldosterone antagonist, slightly reversed the renal reflect when given during maximum action of ASA. Ethacrynic acid could display its full diuretic action unhindered during maximum ASA action. Above observations lead to the suggestion that acetylsalicylic acid might release aldosterone and the action on electrolyte excretion may be mediated by the mineralocorticoid.
