eprosartan and Atherosclerosis

It is clear that the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) play key roles in sustaining elevated blood pressure, subsequently resulting in increased risks of cardiovascular (CV), cerebrovascular and kidney disease. Modifying these systems with antihypertensive agents has led to the discovery that their effects may indeed extend beyond controlling blood pressure. Within blood vessels, angiotensin II type 1 receptor blockers (ARBs) inhibit postsynaptic angiotensin II type 1 receptors (AT1). The ARB eprosartan, in contrast to other ARBs, also inhibits prejunctional AT1 receptors, which regulate noradrenaline release. The positive effects of eprosartan on blood pressure have been studied extensively, and are due to modulation of both the RAS and the SNS (through stimulation of the angiotensin II type 2 [AT2] receptor). Of importance to isolated systolic hypertension, trough sitting systolic blood pressure (SBP) is also significantly reduced with eprosartan. In addition, many studies have shown how the benefits of eprosartan go beyond that of blood pressure control alone. Eprosartan has shown positive effects on vascular inflammation and resistance to oxidation and/or modification of low-density lipoprotein. A wealth of other positive actions are associated with eprosartan treatment, including effects on platelet aggregation, kidney function and structure, progressive left ventricular dysfunction and central SBP. Clinical studies have clearly demonstrated the benefits of RAS blockade alongside the additional effects beyond blood pressure control with eprosartan treatment. These data place eprosartan as an effective agent to prevent CV, cerebrovascular and renal complications associated with high blood pressure.

Topics: Acrylates; Angiotensin II Type 1 Receptor Blockers; Antihypertensive Agents; Atherosclerosis; Humans; Imidazoles; Kidney Diseases; Platelet Aggregation; Renin-Angiotensin System; Sympathetic Nervous System; Thiophenes; Ventricular Dysfunction, Left