How it works

Midodrine hydrochloride forms an active metabolite, desglymidodrine, that is an α-1-agonist, and exerts its actions via activation of the alpha-adrenergic receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of blood pressure. Desglymidodrine does not stimulate cardiac beta-adrenergic receptors.
Desglymidodrine diffuses poorly across the blood-brain barrier and is therefore not associated with effects on the central nervous system.
Administration of Midodrine hydrochloride results in a rise in standing, sitting, and supine systolic and diastolic blood pressure in patients with orthostatic hypotension of various etiologies. Standing systolic blood pressure is elevated by approximately 15 to 30 mmHg at 1 hour after a 10 mg dose of midodrine, with some effect persisting for 2 to 3 hours. Midodrine hydrochloride has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure.