Objective -The ideal antihypertensive agent must have the following profile: it must promote effective blood pressure (BP) reduction, maintain blood pressure control over 24 hours with a single daily dose, be as effective as possible for a great number of hypertensive patients, cause no undesirable side effects have no negative effects on metabolic parameters 1 , and finally be reasonably affordable. None of the antihypertensive agents currently available have all of these characteristics. More recently, some new drugs have demonstrated some of the desired characteristics of an ideal drug.The maintenance of blood pressure reduction during the first hours of the morning, after the patient wakes up, is another major point to be considered, because the most likely peak time for cardiovascular events occurs between 06:00-11:00 2-5 . The goals for blood pressure levels have become increasingly rigorous. The new goals are based on the results from the most recent prospective clinical studies, such as HOT 6 and UKPDS 7 , which demonstrate that more rigorous blood pressure control provides greater protection against cardiovascular morbidity and mortality in hypertensive populations. These findings emphasize that antihypertensive agents must keep blood pressure under control for the longest period of time possible.The renin-angiotensin system (RAS) plays an important role in the pathogenesis and maintenance of the mechanisms involved in the development of essential hypertension. Some of its actions have been well characterized 8 . Briefly, angiotensin II (AII) acts by binding to its specific subtype AT 1 receptor, leading to vasoconstriction, increasing peripheral resistance (raising blood pressure levels), and promoting some trophic actions (wall and heart vessels hypertrophy).A new class of antihypertensive agents, the angiotensin II (AII) antagonist receptors (AIIAR) (ie, losartan, valsartan, irbesartan, candesartan, and telmisartan), blocks the binding of AII to its subclass receptor AT 1 . This action prevents the potent vasoconstriction generated by AII.