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

Laboratoire d'Etude de la Microcirculation, Département de Biophysique, Hôpital Fernand Widal, Cedex 10, Paris 75010, France

Submitted 19 September 2002 ; accepted in final form 15 April 2003

We studied in vivo interactions of nitric oxide (NO), oxidative stress, and prostanoids derived from the cyclooxygenase pathway in the arterioles studied by intravital microscopy in peripheral muscle. Topical administration of NO synthase (NOS) inhibitor N-nitro-L-arginine (L-NNA) or cyclooxygenase inhibitor mefenamic acid (MA) alone leads to vasoconstriction. We found that L-NNA after MA induced an additional constriction, whereas MA after L-NNA induced a relative dilation. Therefore, an additional constriction was found when MA was administered after L-NNA in the presence of the thromboxane A₂ synthase-PGH₂ (TP) receptor antagonist SQ-29548. We also found a relative dilation when the TP receptor antagonist was administered after NOS inhibition by L-NNA. In the presence of superoxide dismutase and catalase, L-NNA-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 favor of constrictor prostanoids. This effect of NO inhibition disappears when reactive oxygen species are scavenged by superoxide dismutase and catalase.

prostaglandins; oxidative stress; microcirculation; vascular reactivity

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