Affiliation:
1. Department of Cell Biology and Neuroscience, Rutgers, State University of New Jersey, Piscataway, New Jersey 08854
Abstract
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.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
19 articles.
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