Effects of oxyfedrine on isolated portal vein and other smooth muscles

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Abstract
Summary: Oxyfedrine (001–1·0 μg/ml), inhibited spontaneous myogenic activity in rat isolated portal vein and carbachol‐induced contractions of rat isolated uterus, and relaxed the rabbit duodenum and the guinea‐pig tracheal chain preparation. These actions were prevented by the β‐adrenoceptor blocking drug alprenolol. Oxyfedrine was a relatively weak β‐adrenoceptor stimulant (10–100 times less active than isoprenaline) but its actions were more prolonged. In the same concentrations, oxyfedrine reduced or prevented the inhibition of myogenic activity of the rat portal vein induced by isoprenaline and by repeated doses of oxyfedrine itself, acting as a partial agonist at β‐adrenoceptor sites. Oxyfedrine, 1–12 μg/ml increased myogenic activity in the rat portal vein. This effect was not due to direct or indirect stimulation of α‐adrenoceptors (because it was unaffected by phentolamine) or to potentiation of acetylcholine or 5‐hydroxytryptamine. Oxyfedrine (>20 μg/ml) inhibited spontaneous myogenic activity in the portal vein and relaxed the saphenous vein contracted with noradrenaline. This spasmolytic effect of the drug was not due to β‐adrenoceptor stimulation or to inhibition of phosphodiesterase since it was unaffected by alprenolol and by concentrations of imidazole which antagonized the effects of the active phosphodiesterase inhibitor, papaverine. In the portal vein this effect of oxyfedrine was similar to that of the calcium inhibitor iproveratril; some of the effects of oxyfedrine on venous smooth muscle may be mediated through effects on calcium transport.