In certain conditions, renal prostaglandins (PGs) are important determinants of kidney function. Under these "renal PG-dependent states," pharmacological inhibition of vasodilatory PG may result in excessive renal vasoconstriction and adversely affect kidney function. The purposes of this study were to determine whether acetaminophen (Acet), a weak PG-synthesis inhibitor, influences kidney function in the renal PG-dependent state of anesthesia and sodium depletion. Comparisons were made with ibuprofen (Ibu). Measurements of PGE₂ excretion were used to assess renal PG synthesis. Acet (15 mg/kg) and Ibu (10 mg/kg) both decreased renal blood flow and glomerular filtration rate by ~20-30% in normal, anesthetized, sodium-replete dogs. Although Acet produced similar changes in renal blood flow and glomerular filtration rate in the low-sodium dogs, Ibu caused a significantly greater renal vasoconstriction (64 ± 10%) in these animals. Both Acet and Ibu inhibited urinary PGE₂ excretion in sodium-replete and low-sodium dogs. Ibu tended to have a greater and more prolonged effect than did Acet. These results suggest that Acet alters PGE₂ excretion and kidney function under renal PG-dependent conditions; the effects, however, are less severe than those seen with Ibu.

prostaglandins; glomerular filtration rate; renal blood flow; sodium depletion

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