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Am J Physiol Heart Circ Physiol (May 1, 2003). doi:10.1152/ajpheart.00839.2002
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Submitted on September 19, 2002
Accepted on April 15, 2003

Interaction between nitric oxide and prostanoids in arterioles of rat cremaster muscle in vivo

Elisabeth Laemmel1, Evelyne Bonnardel-Phu1, Xin Hou1, Julien Seror1, and Eric Vicaut1*

1 Departement de Biophysique, Laboratoire d'Etude de la Microcirculation, Paris, France, Metropolitan

* To whom correspondence should be addressed. E-mail: eric.vicaut{at}lrb.ap-hop-paris.fr.

We studied in vivo interactions of nitric oxide, oxidative stress and prostanoids derived from the cyclooxygenase pathway in the arterioles studied by intravital microscopy in peripheral muscle. Topical administration of NO synthase inhibitor L-N{omega}-nitroarginine (L-NOARG) or cyclooxygenase inhibitor mefenamic acid (MA) alone leads to vasoconstriction. We found that L-NOARG after MA induced an additional constriction whereas MA after L-NOARG induced a relative dilation. Therefore an additional constriction was found when MA was administered after L-NOARG in the presence of the TP receptor antagonist SQ 29548. We also found a relative dilation when the TP receptor antagonist was administered after NOS inhibition by L-NOARG. In the presence of superoxide dismutase and catalase, L-NOARG-induced vasoconstriction is reduced, and the dilation observed after addition of MA in presence of the reactive oxygen species is no longer present. Taken together, these results showed that NO inhibition induced a shift in the synthesis or in the effects of cyclooxygenase products, in favour of constrictor prostanoids. This effect of NO inhibition disappears when reactive oxygen species are scavenged by SOD and catalase.




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