Synephrine hydrochloride

Synephrine hydrochloride (Oxedrine, p-Synephrine) is a sympathomimetic alpha-adrenergic receptor (AR, alpha-adrenoceptor) agonist. Synephrine is ca.40, 000-fold less potent than norepinephrine with respect to binding to beta-1 and beta-2 adrenoreceptors. Synephrine is ca.1000-fold less active than norepinephrine in binding to rat aorta alpha-1 and rabbit saphenous vein alpha-2 adrenoreceptors. Acute intravenous administration of Synephrine reduces portal pressure and increases arteial pressure in portal vein stenosed rats in a dose dependent manner. Synephrine has been administered clinically to shock patients with effective pressor effects. In healthy human volunteers and anesthetized dogs, acute infusion of Synephrine induces both systemic pressor and positive inotropic effects, suggesting activation of both vascular alpha-adrenoceptors and myocardial beta-adrenoceptors. Whereas repeated gavage administration of Synephrine into portal hypertensive and cirrhotic rats results in predominant activation of vascular alpha-adrenoceptors. Synephrine significantly ameliorates the portal hypertension and systemic as well as splanchnic hyperemic state in portal hypertensive rats induced by either partial portal vein ligation (PVL) or bile duct ligation (BDL) through splanchnic vasoconstriction, and exerts beneficial hemodynamic effects in the two models. Synephrine treatment potently leads to constriction of isolated rat aorta in a dose-dependent manner specifically via adrenergic and serotonergic (5-HT1D and 5-HT2A) receptors. Synephrine is a partial agonist of alpha(1A)-AR subtype, giving a maximal response at 100 uM that is equal to 55.3 % of the L-phenylephrine maximum. Similar to beta-phenethylamine, Synephrine may act as an antagonist rather than an agonist of the pre-synaptic alpha(2A)- and alpha(2C)-AR subtypes present in nerve terminals. Synephrine can stimulate glucose consumption (Glut4-dependent glucose uptake) by stimulating AMPK activity in L6 skeletal muscle cells, independent of insulin-stimulated PI3 kinase-Akt activity.

Oxedrine hydrochloride

C9H13NO2.HCl

>98%