Valtensi Mechanism of Action

Mechanism of Action: The active hormone in the renin-angiotensin aldosterone system (RAAS) is angiotensin II, which is formed from angiotensin I through angiotensin-converting enzyme (ACE). Angiotensin II binds to receptors that is located in cell membranes of various tissues. It has various physiological effects, including direct and indirect involvement in regulating blood pressure. As a powerful vasoconstrictor, angiotensin II increases sodium retention and stimulates aldosterone secretion. Valsartan in oral active form, strong and specific to angiotensin II (Ang II) antagonist receptors. It acts selectively on the AT1 receptor subtype which is responsible for all the effects of angiotensin II. Increased plasma levels of Ang II accompanied by AT1 blockade by valsartan can stimulate unblocked AT2 receptors, which appear to offset the effects of AT1 receptors. Valsartan does not exhibit any partial agonist activity at the AT1 receptor and has much (about 20,000 fold) greater affinity for the AT1 receptor than for the AT2 receptor. Valsartan does not inhibit ACE, also known as kinase II, which converts Ang I to Ang II and decreases bradykinin. Because there is no effect on ACE and no potentiation of bradykinin and P substance, coughing is not caused by angiotensin II antagonists. Valsartan is not bound or block other hormone receptors or Ion channels which play an important role in cardiovascular regulation.