||Renin is an aspartyl protease of approximately 40 kDa. It is released in an active form from the renal juxtaglomerular cells in response to physiologic factors, including sodium depletion, decreased blood volume and blood pressure, and β-adrenergic stimulation. Renin converts angiotensinogen into angiotensin I. Angiotensin converting enzyme (ACE), a monomeric zinc metalloenzyme found in the vascular endothelium, then converts this pro-hormone to angiotensin II, the final active messenger in the renin-angiotensin system(RAS) pathway.2,3 Angiotensin II inhibits renin secretion by acting directly on the juxtaglomerular cells. Angiotensin II has a number of physiological effects, most importantly as a powerful vasoconstrictor, increasing blood pressure by altering peripheral vascular resistance. Since angiotensinogen is the only known substrate for renin and cleavage of angiotensinogen by renin is the rate determining step in the RAS pathway, it is of general consensus that inhibition of renin would be an attractive strategy for the control of hypertension. Furthermore, renin inhibitors would prevent the formation of angiotensin I and angiotensin II, and, therefore, may act differently from angiotensin receptor blockers and ACE inhibitors, which increase angiotensin I levels but do not block ACE-independent angiotensin II production.