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Irbesartan stops angiotensin II binding to your AT1 receptor in tissues like vascular sleek muscle as well as the adrenal gland. Irbesartan and its Lively metabolite bind the AT1 receptor with 8500 moments additional affinity than they bind on the AT2 receptor.

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Irbesartan isn't going to inhibit ACE or renin or influence other hormone receptors or ion channels known for being involved in the cardiovascular regulation of hypertension and sodium homeostasis.

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Blockade with the AT1 receptor eliminates the destructive feed-back of angiotensin II on renin secretion, but the ensuing improved plasma renin exercise and circulating angiotensin II don't triumph over the results of irbesartan on hypertension.

The renin-aldosterone link is mediated by angiotensin II, so coadministration of the angiotensin II receptor antagonist tends to reverse the potassium decline connected to these diuretics.