USP(U.S. Pharmacopeia / National Formulary)
17-HYDROXYYOHIMBAN-16-CARBOXYLIC ACID METHYL ESTER HYDROCHLORIDE;17A-HYDROXYYOHIMBAN-16A-CARBOXYLIC ACID METHYL ESTER HYDROCHLORIDE;YOHIMBE HCL;YOHIMBINE HCL;YOHIMBINE HYDROCHLORIDE;QUERBRACHINE;17alpha)-alph;Yohimban-16-alpha-carboxylic acid, 17-alpha-hydroxy, methyl ester, monohydrochloride
white to off-white powder
Yohimbine hydrochloride is an α2-adrenergic receptor antagonist and increases the firing rate of the locus coeruleus with a resultant increase in sympathetic outflow (Redmond, 1987). Oral and intravenous yohimbine causes an increase in MHPG and blood pressure in healthy human subjects (Charney et al., 1982d; Goldberg et al., 1986). Depressed patients demonstrate an increased cortisol and blood pressure response to intravenous yohimbine compared with healthy subjects, while plasma MHPG is not significantly different between the two groups of subjects (Heninger et al., 1988). The effects of acute or chronic antidepressant treatments on the neuroendocrine or behavioural responses to yohimbine in depressed patients have not been studied.
Yohimbine hydrochloride—an α2-adrenoceptor antagonist that is approved for treatment of erectile dysfunction—may increase BP.1,2,In normal volunteers and in patients with panic disorders, oral administration at doses used clinically may slightly increase BP.1 However, in hypertensive patients oral yohimbine was reported to induce a significant increase in mean arterial pressure.The magnitude of the pressor response was related to baseline norepinephrine levels and to the yohimbine-induced increment in plasma norepinephrine levels.Thus yohimbine increases BP by stimulation of the sympathetic nervous outflow, and the drug should be administered with caution to patients with evidence for increased basal sympathetic outflow or those undergoing concurrent treatment with tricyclic antidepressants or other drugs that interfere with neuronal uptake or metabolism of norepinephrine.