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Department of Physiology, School of Medicine, University of Murcia, 30100 Murcia, Spain
The aim of this study was to examine
the relative contribution of both cyclooxygenase (COX) isoforms in
producing the prostaglandins (PG) involved in the regulation of renal
function, when nitric oxide (NO) synthesis is reduced. In anesthetized
dogs with reduction of NO synthesis, the renal effects of a
nonisozyme-specific COX inhibitor (meclofenamate) were compared with
those elicited by a selective COX-2 inhibitor (nimesulide) before
and during an extracellular volume expansion (ECVE). Intrarenal
NG- nitro-L-arginine methyl
ester (L-NAME) infusion (1 µg · kg
1 · min1;
n = 6) did not elicit renal hemodynamic changes and
reduced (P < 0.01) the renal excretory response to
ECVE. Intravenous nimesulide (5 µg · kg1 · min1;
n = 6) did not modify renal hemodynamic and reduced
(P < 0.05) sodium excretion before ECVE. Simultaneous
L-NAME and nimesulide infusion (n = 7)
elicited an increment (37%) in renal vascular resistance (RVR;
P < 0.05) before ECVE and no hemodynamic changes during ECVE. The reduced excretory response elicited by
L-NAME and nimesulide was similar to that found during
L-NAME infusion. Finally, simultaneous L-NAME
and meclofenamate infusion (10 µg · kg1 · min1;
n = 7) induced an increase in RVR (91%,
P < 0.05), a decrease in glomerular filtration rate
(35%, P < 0.05), and a reduction of the renal
excretory response to ECVE that was greater (P < 0.05)
than that elicited by L-NAME alone. The results obtained support the notion that PG involved in regulating renal hemodynamic and
excretory function when NO synthesis is reduced are mainly dependent on
COX-1 activity.
sodium excretion; renal hemodynamic
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