Olmesartan Medoxomil + Hydrochlorothiazide

Angiotensin-II is formed from angiotensin-I in a reaction catalyzed by angiotensin-converting enzyme (ACE). It is a potent vasoconstrictor, the primary vasoactive hormone of the renin-angiotensin system, and an important part of how hypertension develops. It also stimulates the adrenal cortex to secrete aldosterone.

Olmesartan, the first component of Olmesartan Medoxomil + Hydrochlorothiazide, blocks both the vasoconstrictor effect and the aldosterone-secreting effect of angiotensin-II. It does this by selectively blocking angiotensin-II from binding to the AT 1 receptor, which is found in many tissues (for example vascular smooth muscle and the adrenal gland). In-vitro-binding studies show that Olmesartan is a reversible and competitive inhibitor of the AT 1 receptor. It does not inhibit ACE (kinase-I), the enzyme that converts angiotensin-I to angiotensin-II and also breaks down bradykinin.

Hydrochlorothiazide is a thiazide diuretic. Thiazides act on the mechanisms in the renal tubules that reabsorb electrolytes, and they directly increase the excretion of Sodium and Chloride in approximately equivalent amounts. Indirectly, the diuretic action of Hydrochlorothiazide reduces plasma volume. This raises plasma renin activity, increases Aldosterone secretion and urinary Potassium loss, and lowers serum Potassium. Angiotensin-II mediates the link between renin and aldosterone, so giving an angiotensin-II receptor antagonist together with the diuretic tends to reverse the potassium loss these diuretics cause.