Valsartan is an orally active and powerful angiotensin II receptor antagonist. It acts specifically on the receptor subtype AT1, which is in charge of the known activities of angiotensin II. The increased plasma levels of angiotensin II following AT1 receptor bar with valsartan may activate the unblocked receptor subtype AT2, which seems to offset the impact of the AT1 receptor.
Valsartan does not display any incomplete agonist activity at the AT1 receptor and has much affinity for the AT1 receptor than for the AT2 receptor. Valsartan does not hinder ACE, otherwise called kininase II, which changes over angiotensin I to angiotensin II and degrades bradykinin. Since there is no impact on ACE and no potentiation of bradykinin or substance P, angiotensin II antagonists do not give rise to cough.
Giving valsartan to patients with hypertension results in a drop in blood without influencing heart rate.
Amlodipine relaxes smooth muscles in the heart and blood vessels. It produces coronary vasodilation by restraining the passage of calcium ions into the slow channels or selected voltage-sensitive channels of the vascular smooth muscle and myocardium amid depolarisation. It additionally increases myocardial oxygen delivery in patients with vasospastic angina or chest pain.
