Noxidil/Noxidil Forte Mechanism of Action

Pharmacology: Pharmacodynamics: Minoxidil is a direct-acting peripheral vasodilator. It does not interfere with vasomotor reflexes; therefore, it does not produce orthostatic hypotension. The drug does not affect CNS function.
Because it causes peripheral vasodilation, minoxidil elicits a reduction of peripheral arteriolar resistance. This action, with the associated fall in blood pressure, triggers sympathetic, vagal inhibitory, and renal homeostatic mechanisms, including an increase in renin secretion, which leads to increased cardiac rate and output, and salt and water retention. These adverse effects can usually be minimized by coadministration of a diuretic and a beta-adrenergic-blocking agent or other sympathetic nervous system suppressant.
Antihypertensive effects: Minoxidil reduces elevated systolic and diastolic blood pressure by decreasing peripheral vascular resistance. The blood pressure response to minoxidil is dose-related and proportional to the extent of hypertension. In humans, forearm and renal vascular resistance decline; forearm blood flow increases while renal blood flow and glomerular filtration rate (GFR) are preserved.
Pharmacokinetics: Absorption/Distribution: Minoxidil is not protein bound and is at least 90% absorbed from the GI tract. Plasma levels of the parent drug reach a maximum within the first hour and decline rapidly thereafter.
Metabolism/Elimination: Predominantly by conjugation with glucuronic acid, 90% is metabolized. Metabolites exert much less pharmacologic effect than minoxidil itself; all are excreted principally in the urine. Renal clearance corresponds to the GFR. Minoxidil and its metabolites are hemodialyzable. Average plasma half-life is 4.2 hours.