Modulation of sympathetic constriction by the arteriolar endothelium does not involve the cyclooxygenase pathway.

Abstract

We have recently shown that the responsiveness of rat intestinal arterioles to increased sympathetic nerve activity is modulated by the actions of endothelial-derived nitric oxide. Because the microvascular endothelium can also produce vasodilator prostaglandins, the purpose of this study was to determine if endogenous cyclooxygenase products also limit sympathetic arteriolar constriction in this vascular bed. Intravital microscopy was used to study the responses of small feed arteries, first-order arterioles and second-order arterioles to perivascular sympathetic nerve stimulation in the superfused rat small intestine. Stimulation at 3, 8 and 16 Hz caused frequency-dependent constrictions of each vessel type that are abolished by the alpha-adrenoceptor antagonist phentolamine (10(-6) M superfusate concentration). The cyclooxygenase inhibitor meclofenamate (3 x 10(-5) M superfusate concentration) completely abolished the dilator responses to topically applied arachidonic acid, but had no effect on the magnitude or rate of sympathetic constriction in any vessel type. These results suggest that endogenous cyclooxygenase activity does not influence sympathetic tone in the intestinal microvasculature.