Naloxone selectively inhibits vasoconstriction caused by phenylephrine but not endogenous noradrenaline in the rat mesenteric vasculature.

Abstract

Although naloxone is an antagonist of the opioid µ receptor, its effect on the peripheral sympathetic nerve function in the blood vessels has not yet been definitively elucidated. Therefore, we examined the effects of naloxone on vasoconstriction of the vascular smooth muscle of rats. Isolated rat mesenteric vascular-intestinal loop preparations were treated with either endogenous or exogenous α₁ adrenoceptor agonists followed by prazosin, a selective antagonist of the α₁ adrenoceptor, or naloxone, and noradrenaline overflow was measured. Vasoconstriction caused by peri-arterial nerve stimulation (PNS) and phenylephrine, an exogenous agonist of the α₁ adrenoceptor, was abolished by prazosin. However, prazosin did not affect PNS-induced endogenous noradrenaline overflow. Naloxone did not affect either PNS-induced endogenous noradrenaline overflow or vasoconstriction. However, naloxone did inhibit phenylephrine-induced vasoconstriction. In addition, naloxone did not affect the angiotensin II-induced vasoconstriction. These results demonstrate that naloxone selectively inhibits vasoconstriction caused by phenylephrine, but not vasoconstriction caused by endogenous noradrenaline released from sympathetic nerve cells in the rat mesenteric vasculature.