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Pleiotropic Effects of Inhibitors of the RAAS in the Diabetic Population: Above and Beyond Blood Pressure Lowering

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Abstract

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are indispensable therapeutic agents for treating hypertension and proteinuria in patients with diabetes mellitus. Studies have shown that the renin-angiotensin-aldosterone system (RAAS) has effects on various organ systems, including the central nervous system, heart, and kidneys. Angiotensin II has major deleterious effects on vascular compliance, vascular relaxation, and plasma markers of inflammation, which are surrogate markers of cardiovascular disease. Evidence is established from major trials that ACE inhibitors and ARB therapy improve these surrogate markers and reduce cardiovascular disease, renal disease, and stroke. Accumulating evidence also supports the newer class of medication, the direct renin inhibitor aliskiren, as beneficial in hypertensive persons with diabetes mellitus. In this article, we review the mechanisms through which inhibitors of the RAAS benefit persons with hypertension and decrease the development of cardiovascular and renal disease above and beyond blood pressure lowering.

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Abbreviations

ALLAY:

Aliskiren Left Ventricular Assessment of Hypertrophy

ALOFT:

Aliskiren Observation of Heart Failure Treatment

ALTITUDE:

Aliskiren Trial in Type 2 Diabetes Using Cardiovascular and Renal Disease Endpoints

AVOID:

Aliskiren in the Evaluation of Proteinuria in Diabetes

CAPPP:

Captopril Prevention Project

HOPE:

Heart Outcomes Prevention Evaluation

MICRO-HOPE:

Microalbuminuria, Cardiovascular and Renal Outcomes

ONTARGET:

Ongoing Telmisartan Alone and in Combination With Ramipril Global Endpoint Trial

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Correspondence to Amgad N. Makaryus.

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Ismail, H., Mitchell, R., McFarlane, S.I. et al. Pleiotropic Effects of Inhibitors of the RAAS in the Diabetic Population: Above and Beyond Blood Pressure Lowering. Curr Diab Rep 10, 32–36 (2010). https://doi.org/10.1007/s11892-009-0081-y

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