Renin-Angiotensin-aldosterone system in diabetes and hypertension

Abstract

Activation of the renin-angiotensin-aldosterone system (RAAS) is the primary etiologic event in the development of hypertension in people with diabetes mellitus. Modulation of the RAAS has been shown to slow the progression and even cause regression of the microvascular and macrovascular complications associated with diabetes mellitus. Early pharmacotherapy with agents that decrease RAAS activation in the adipose tissue have had a dramatic impact on the prevalence of diabetes related complications. Recent data show that preventing the development of "angry fat" can prevent not just hypertension but also type 2 diabetes mellitus and its associated complications. This review updates what is known about angry fat and the role of RAAS inhibition in preventing the metabolic sequelae of local RAAS activation.

Figure 1

Adipose is an endocrine organ. Adipose tissue produces adipokines that send signals to many organs to maintain basic metabolic functions. IL‐6 = interleukin‐6; CRP = C‐reactive protein; TNFα = tumor necrosis factor‐alpha.

Figure 2

Targets of angry fat. Activation of the RAAS in adipose tissue is associated with an increase in production of cytokines that communicate the health of the adipose tissue to the nonadipose organs throughout the body. PAI‐1 = plasminogen activator inhibitor 1; PPARs = peroxisome proliferators‐activated receptors; RXR = retinoid × receptor; LVH = left ventricular hypertrophy.