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

Author:

Beierwaltes William H.1

Affiliation:

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

Abstract

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. Afterl-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.

Publisher

American Physiological Society

Subject

Physiology

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