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Am J Physiol Renal Physiol 283: F68-F72, 2002. First published February 12, 2002; doi:10.1152/ajprenal.00364.2001
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Vol. 283, Issue 1, F68-F72, July 2002

Cyclooxygenase-2 products compensate for inhibition of nitric oxide regulation of renal perfusion

William H. Beierwaltes

Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Michigan 48202-2689

Cyclooxygenase (COX)-2 is in the macula densa, cosegregating with neuronal nitric oxide synthase (nNOS). It is hypothesized that in response to acute inhibition of NOS, the influence of COX-2-derived prostanoids is exaggerated, compensating for renal vasoconstriction. Blood pressure (BP) and renal blood flow (RBF) were measured after selective COX-2 inhibition with NS-398 followed by NOS inhibition with L-nitro arginine methyl ester (L-NAME) or after L-NAME followed by NS-398. BP was 106 ± 4 mmHg and was unaffected by NS-398. L-NAME after NS-398 increased BP by 27 ± 2 mmHg, decreased RBF by one-half, and doubled renal vascular resistance (RVR; P < 0.001). Initial L-NAME increased BP by 26 ± 3 mmHg (P < 0.001) and decreased RBF by 44% (P < 0.001), doubling RVR. After L-NAME, NS-398 induced a further 7 ± 3-mmHg rise in BP (P < 0.05), decreased RBF by 20% (P < 0.025), and increased RVR by 23% (P < 0.01). The constrictor response to COX-2 inhibition after L-NAME could not be duplicated by either selective nNOS inhibition or NOS-independent renal vasoconstriction. Acute NOS inhibition unmasked renal vasoconstriction with COX-2 inhibition, suggesting that the influence of COX-2-derived vasodilator eicosanoids is exaggerated to maintain renal perfusion, compensating for the acute loss of NO.

renal blood flow; prostaglandins; neuronal nitric oxide synthase; endothelial nitric oxide synthase; renal vasoconstriction


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