Clinical investigations into the use of Angiotensin-Converting Enzyme (ACE) inhibitors to slow the effects of diabetic nephropathy and the subsequent use of angiotensin II receptor blockers (ARBs) to reduce the progressive decay of GFR in Chronic kidney disease (CKD) to treat diabetes mellitus type 1 and type 2 have shown significant progress (Turner, Bauer, Abramowitz, Melamed & Hostetter, 2012). According to Ferrario and Strawn (2006), activating the Renin-Angiotensin-Aldosterone system (RAAS) inhibitors, the direct results of systematic capillary hypertension, promote pathologic effects which induce hemodynamic injury to the glomerulus and vascular endothelium. RAAS inhibitors are crucial for stabilizing or reducing proteinuria and for slowing the progress of renal injury in patients diagnosed with macroalbuminuria and microalbuminuria. A recent meta-analysis report by Turner et. al., (2012) and results from AASK trials on the prevalence of hypertensive nephropathy in African Americans shows that RAAS inhibitors have a strong positive action on patients diagnosed with the non-diabetic renal disease with a >1000 mg/day proteinuria. Turner et. al., (2012) argues that there is no empirical evidence to show that RAAS and ACE inhibitors reduce the progress of autosomal dominant polycystic kidney disease, the toxic levels of proteinuria, and the existence of a relationship between renal injury and proteinuria.
According to Ferrario and Strawn (2006), clinical sequelae of cardiovascular diseases and inflammation underpin the actions of hemodynamic/antihypertensive and anti-inflammatory/antifibrotic. The actions are widely accepted mechanisms that ARB and ACE inhibitors used to control CKD (Turner et. al., 2012). The hemodynamic/antihypertensive and anti-inflammatory/antifibrotic actions are achieved by suppressing angiotensin II receptor blockers and angiotensin II using angiotensin-converting enzyme inhibitors or by reversing atherosclerosis to elevate glomerular capillary pressures. The results include a reduction in adverse cardiovascular events, lower blood pressure, and CKD progress. Turner et. al., (2012) argues that suppressing RAAS reduces femoral artery intima-media thickness and common carotid, and the progress of vascular diseases through the proinflammatory and profibrotic mediators. Clinical investigations show that the high concentration of angiotensin II in the kidney which is caused by the activation of NF-κB with a nuclear factor κ-light-chain-enhancer, fosters fibrosis by interacting with the transforming growth factor-β, type I procollagen fibronectin, and collagen’s type IV extracellular matrix proteins. The mechanism slows down the progress of CKD (Ferrario & Strawn, 2006).
Clinical trials show that the renin-angiotensin-aldosterone system (RAAS) and renin-angiotensin system (RAS) provide a hormonal system for regulating the balance of water and blood pressure. The mechanism for increasing the volume of blood involves activating prorenin in the juxtaglomerular cells to secrete renin, making the blood plasma raise the angiotensinogen levels by converting angiotensin I to angiotensin II. The potent Angiotensin II vasoactive peptide induces the secretion of aldosterone from the adrenal cortex and constricts blood vessels to increase the blood pressure in the vessels (Ferrario & Strawn, 2006).
A schematic concordance of (RAAS) shows the potent effects of angiotensin II on blood pressure and the ‘in vitro’ evidence of mitogenic actions on the growth of myocardial fibroblast. That allows for the development of standard drugs and primary hypertension to slow the activity of kidney disease.
In conclusion, Renin-Angiotensin-Aldosterone System (RAAS) including Angiotensin Receptor Blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors provide effective clinical control of kidney tissue growth and the potent effects of angiotensin II in patients with renal and cardiovascular disorders.
References
Ferrario, C. M. & Strawn, W. B. (2006). Role of the renin-angiotensin-aldosterone system and proinflammatory mediators in cardiovascular disease. American Journal of Cardiology, 98 (1): 121–128.
Turner, J. M., Bauer,C., Abramowitz, M. K., Melamed, M. L. & Hostetter, T. H (2012). Treatment of Chronic Kidney Disease. Web.