Produção Nacional
Revisado por pares
CYCLOOXYGENASE INHIBITION REDUCES BLOOD PRESSURE ELEVATION AND VASCULAR REACTIVITY DYSFUNCTION CAUSED BY INHIBITION OF NITRIC OXIDE SYNTHASE IN RATS
2000; Informa; Volume: 22; Issue: 2 Linguagem: Inglês
10.1081/ceh-100100073
ISSN1525-6006
AutoresValdeci da Cunha, Luciana Venturini Rossoni, Patrícia Oliveira, Silmara Poton, Silvio Cesar Pretti, Dalton Valentim Vassallo, Ivanita Stefanon,
Tópico(s)Hormonal Regulation and Hypertension
ResumoIn 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 L-NAME 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 (10−4M) in normal rat aortas were not modified by indomethacin (10−5M). 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.
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