Abstract
Abstract
The pharmacological properties of naloxone on vascular smooth muscle in vitro were examined using canine mesenteric arterial segments. Naloxone exerted two different effects on the artery: (A) naloxone at a high concentration (3 × 10-4 M) produced a nonspecific vasodilation; and (B) naloxone at lower concentrations (3 × 10-7, 3 × 10-6, and 3 × 10-5 M) augmented the vasoconstrictor effects of epinephrine and norepinephrine without altering KCl-or serotonin-induced constriction. Naloxone's augmenting effect on epinephrine-induced constriction was dose dependent. Even when the arterial strips were incubated in low calcium (0.8 mM) or calcium free Kreb's solution, naloxone (3 × 10-5 M) still augmented epinephrine-induced constriction. With respect to naloxone's effect on another α-adrenoreceptor agonist, naloxone (3 × 10-5 M) failed to alter phenylephrine-induced constriction. Naloxone's augmenting effect on norepinephrine-induced constriction was abolished when the specimens were incubated with 10-5 M normetanephrine, while naloxone (3 × 10-5 M) still augmented the constriction even when the specimens were incubated with 10-5 M cocaine. These results suggest that naloxone at lower concentrations may augment the constrictor responses to catecholamines, at least in part, by inhibiting the extraneuronal uptake of those catecholamines.
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