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Articles in PresS, published online ahead of print February 12, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00364.2001
Submitted on December 13, 2001
Accepted on February 8, 2002
1 Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: wbeierw1{at}hfhs.org.
Cyclooxygenase 2 (COX-2) is in the macula densa cosegregating with neuronal nitric oxide synthase (NOS). It is hypothesized that in response to acute inhibition of NOS, the influence of COX-2-derived prostanoids is exaggerated, compensating for renal vasoconstriction. We measured blood pressure (BP) and renal blood flow (RBF) after either selective COX-2 inhibition with NS-398 followed by NOS inhibition with L-NAME, or L-NAME followed by NS-398. BP was 106±4 mmHg and unaffected by NS-398. L-NAME after NS-398 increased BP 27±2 mmHg, decreased RBF by half and doubled renal vascular resistance (RVR)(p<0.001). Initial L-NAME increased BP 26±3 mmHg (p<0.001) decreased RBF 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 20% (p<0.025) and RVR increased 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 the influence of COX-2-derived vasodilator eicosanoids is exaggerated to maintain renal perfusion, compensating for the acute loss of NO.
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