Midodrine is converted to its active metabolite, desglymidodrine by deglycination reaction. Desglymidodrine selectively binds to and activates alpha-1-adrenergic receptors of the arteriolar and venous vasculature. This causes smooth muscle contraction and leads to an elevation of blood pressure. Desglymidodrine diffuses poorly across the blood-brain barrier and is therefore not associated with effects on the central nervous system. Midodrine hydrochloride (Pro-Amatine) is the hydrochloride salt form of midodrine, a direct-acting prodrug and sympathomimetic agent with antihypotensive properties.