Olmesartan Medoxomil

Angiotensin II, the main pressor hormone of the renin-angiotensin system, is produced from angiotensin I through the action of angiotensin-converting enzyme (ACE, also known as kininase II). It acts on blood vessels to cause constriction, prompts the adrenal glands to synthesize and release aldosterone, stimulates the heart, and promotes sodium reabsorption by the kidneys.

Olmesartan works by selectively blocking angiotensin II from binding to the AT1 receptor found in vascular smooth muscle, thereby preventing its vessel-constricting effect. A second receptor type, AT2, is also present in many tissues, but it has no established role in cardiovascular regulation. Olmesartan's affinity for the AT1 receptor is more than 12,500 times greater than for the AT2 receptor, making its action highly selective.

Unlike ACE inhibitors, olmesartan medoxomil does not inhibit ACE (kininase II) and therefore does not alter the body's response to bradykinin. By blocking the angiotensin II receptor, olmesartan interrupts the normal feedback mechanism through which angiotensin II suppresses renin release. This leads to a rise in plasma renin activity and circulating angiotensin II levels, but this compensatory increase is not enough to overcome olmesartan's blood-pressure-lowering effect.