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Vol. 289, Issue 2, 735-741, May 1999
The EUPenn Group of Investigators at the Center for Experimental
Therapeutics, Conventional nonsteroidal anti-inflammatory drugs inhibit both
cyclooxygenase (Cox) isoforms (Cox-1 and Cox-2) and may be associated
with nephrotoxicity. The present study was undertaken to assess the
renal effects of the specific Cox-2 inhibitor, MK-966. Healthy older
adults (n = 36) were admitted to a clinical
research unit, placed on a fixed sodium intake, and randomized under
double-blind conditions to receive the specific Cox-2 inhibitor, MK-966
(50 mg every day), a nonspecific Cox-1/Cox-2 inhibitor,
indomethacin (50 mg t.i.d.), or placebo for 2 weeks. All treatments
were well tolerated. Both active regimens were associated with a
transient but significant decline in urinary sodium excretion during
the first 72 h of treatment. Blood pressure and body weight did
not change significantly in any group. The glomerular filtration rate (GFR) was decreased by indomethacin but was not changed significantly by MK-966 treatment. Thromboxane biosynthesis by platelets was inhibited by indomethacin only. The urinary excretion of the
prostacyclin metabolite 2,3-dinor-6-keto prostaglandin
F1
was decreased by both MK-966 and indomethacin and was
unchanged by placebo. Cox-2 may play a role in the systemic
biosynthesis of prostacyclin in healthy humans. Selective inhibition of
Cox-2 by MK-966 caused a clinically insignificant and transient
retention of sodium, but no depression of GFR. Inhibition of both Cox
isoforms by indomethacin caused transient sodium retention and a
decline in GFR. Our data suggest that acute sodium retention by
nonsteroidal anti-inflammatory drugs in healthy elderly subjects is
mediated by the inhibition of Cox-2, whereas depression of GFR is due
to inhibition of Cox-1.
0022-3565/99/2892-0735$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1999 by The American Society for Pharmacology and Experimental Therapeutics
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