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Table 7 The RAAS Acronym: GLOBAL RISK REDUCTION

From: Uric acid: A new look at an old risk marker for cardiovascular disease, metabolic syndrome, and type 2 diabetes mellitus: The urate redox shuttle

R Reductase inhibitors (HMG-CoA). Decreasing modified LDL-cholesterol, i.e., oxidized, acetylated LDL-cholesterol. Decreasing triglycerides and increasing HDL-cholesterol.
Improving endothelial cell dysfunction. Restoring the abnormal Lipoprotein fractions.
Thus, decreasing the redox and oxidative stress to the arterial vessel wall and myocardium.
  Redox stress reduction
A AngII inhibition or receptor blockade:
ACEi-prils. ARBs-sartans. Both inhibiting the effect of angiotensin-II locally as well as systemically. Affecting hemodynamic stress through their antihypertensive effect as well as the deleterious effects of angiotensin II on cells at the local level – injurious stimuli -decreasing the stimulus for O2 production. Decreasing the A-FLIGHT toxicities. The positive effects on microalbuminuia and delaying the progression to end stage renal disease. Plus the direct-indirect antioxidant effect within the arterial vessel wall and capillary. Antioxidant effects.
Aspirin antiplatelet, anti-inflammatory effect on the diabetic hyperactive platelet.
Adrenergic (non-selective blockade) in addition to its blockade of prorenin → renin conversion.
Amlodipine – Felodipine with calcium channel blocking antihypertensive effect, in addition to their direct antioxidant effects.
  Redox stress reduction
A Aggressive control of diabetes to HbA1c of less than 7. This usually requires combination therapy with the use of insulin secretagogues, insulin sensitizers (PPAR-gamma agonists), biguanides, alpha-glucosidase inhibitors, and ultimately exogenous insulin.
Decreasing modified LDL cholesterol, i.e., glycated-glycoxidated LDL cholesterol. Improving endothelial cell dysfunction. Also decreasing glucotoxicity and the oxidative-redox stress to the intima and pancreatic islet.
Aggressive control of blood pressure, which usually requires combination therapy, including thiazide diuretics to attain JNC 7 guidelines.
Aggressive control of homocysteine with folic acid with its associated additional positive effect on re-coupling the eNOS enzyme reaction by restoring the activity of the BH4 cofactor to run the eNOS reaction via a folate shuttle mechanism and once again produce eNO.
Aggressive control of uric acid levels with xanthine oxidase inhibitors (allopurinol and oxypurinol) should be strongly considered in view of the prevailing literature in order to achieve more complete: Global Risk Reduction
  Redox stress reduction
S Statins. Improving plaque stability (pleiotropic effects) independent of cholesterol lowering. Improving endothelial cell dysfunction. Moreover, the direct/indirect antioxidant anti-inflammatory effects within the islet and the arterial vessel wall promoting stabilization of the unstable, vulnerable islet and the arterial vessel wall.
Style. Lifestyle modification (weight loss, exercise, and change eating habits).
Stop Smoking.
  Redox stress reduction