Endogenous prostacyclin increases neuronal nitric oxide release in mesenteric artery from spontaneously hypertensive rats

Abstract

The aim of this study was to analyse the possible influence of endogenous prostacyclin on neuronal nitric oxide (NO) release induced by electrical field stimulation in mesenteric arteries from spontaneously hypertensive rats (SHR). Preincubation with the prostacyclin synthesis inhibitor tranylcypromine decreased NO release induced by electrical field stimulation, which was reversed by exogenous prostacyclin. Preincubation with tranylcypromine increased basal and electrical field stimulation-induced [ 3H]noradrenaline release. The nitric oxide synthase inhibitor N ω -nitro- l-arginine methyl esther ( l-NAME) increased the vasoconstrictor response induced by electrical field stimulation. In the presence of tranylcypromine, l-NAME did not modify the vasoconstrictor response induced by electrical field stimulation. In the presence of tranylcypromine and prostacyclin, l-NAME increased the vasoconstrictor response to electrical field stimulation. These results indicate that endogenous prostacyclin positively modulates the neuronal NO release induced by electrical field stimulation and that this neuronal NO participates in the regulation of the vasomotor response.