title: Systemic hypertension and the renin-angiotensin system in diabetic vascular complications.
abstract: Antihypertensive treatment in the diabetic patient is a critical issue because hypertension has an impact on all of the vascular complications of diabetes, including nephropathy, retinopathy, atherosclerosis, and left ventricular hypertrophy. These complications are a consequence of altered endothelial-vascular smooth muscle interrelations that ultimately enhance vasoconstriction and alter the remodeling processes in the vascular wall. Several observations suggest that the renin-angiotensin system (RAS) may be an important contributor to these processes in diabetes mellitus. In both animal and human studies, angiotensin-converting enzyme (ACE) inhibitors have been demonstrated to slow the progression of glomerulosclerosis, prevent abnormal remodeling processes in the heart following injury, and slow the progression of atherosclerosis. In particular, ACE inhibitors appear to protect the kidney more than would be expected from simply the lowering of blood pressure and decreasing of intraglomerular pressure, possibly because angiotensin II has both hemodynamic and direct effects on the glomerulus. Paradoxically, however, the activity of the circulating RAS is low in diabetic patients. Part of these seemingly inconsistent observations may be due to (1) potential activity of tissue RASs, (2) increased sensitivity to angiotensin II in diabetes, or (3) an effect of ACE inhibition on other systems in addition to the RAS. Investigation of these mechanisms will be important in determining the therapeutic role of inhibition of the RAS in diabetes mellitus.
authors.affiliation: Department of Medicine, University of Southern California, School of Medicine, Los Angeles.
authors.forename: W A
authors.initials: WA
authors.lastname: Hsueh
authors.forename: P W
authors.initials: PW
authors.lastname: Anderson
mesh_terms: D000818:Animals; D003925:Diabetic Angiopathies / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000502:physiology*