CYCLOOXYGENASE INHIBITION REDUCES BLOOD PRESSURE ELEVATION AND VASCULAR REACTIVITY DYSFUNCTION CAUSED BY INHIBITION OF NITRIC OXIDE SYNTHASE IN RATS.

Autor: da Cunha, Valdeci, Rossoni, Luciana V., Oliveira, Patricia A., Poton, Silmara, Pretti, Silvio Cesar, Vassallo, Dalton V., Stefanon, Ivanita
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Zdroj: Clinical & Experimental Hypertension; Feb2000, Vol. 22 Issue 2, p203-215, 13p, 1 Chart
Abstrakt: In the present study we investigated the role of cyclooxygenase (COX)-dependent vasoconstrictors in the hypertension and altered vascular reactivity following prolonged nitric oxide (NO) synthase inhibition. Male Wistar rats (250-270g) were divided into four groups and treated for 7 days with Placebo (control), L-NAME (48 mg/kg/day), indomethacin (4 mg/kg/day) and LNAME in combination with indomethacin. L-NAME treatment induced arterial hypertension, in vitro aortic hyperresponsiveness to phenylephrine, impaired vasodilatory response to acetylcholine and no significant change in response to sodium nitroprusside. Indomethacin co-treatment partially prevented blood pressure elevation, restored responsiveness to phenylephrine and improved sensitivity to acetylcholine. Indomethacin treatment alone did not modify blood pressure and aortic vascular reactivity. Both enhanced phenylphrine-induced contraction and impaired acetylcholine-evoked vasodilation induced by acute NO synthase inhibition with L-NAME (10[sup -4]M) in normal rat aortas were not modified by indomethacin (10[sup -5]M). These results are consistent with the hypothesis that constricting factors, which arise from the COX pathway, contribute to hypertension and altered vascular reactivity following continued inhibition of NO synthase. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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