Small artery remodelling in diabetes.
The aim of this article is to briefly review available data regarding changes in the structure of microvessels observed in patients with diabetes mellitus, and possible correction by effective treatment. The development of structural changes in the systemic vasculature is the end result of established hypertension. In essential hypertension, small arteries of smooth muscle cells are restructured around a smaller lumen and there is no net growth of the vascular wall, although in some secondary forms of hypertension, a hypertrophic remodelling may be detected. Moreover, in non-insulin-dependent diabetes mellitus a hypertrophic remodelling of subcutaneous small arteries is present. Indices of small resistance artery structure, such as the tunica media to internal lumen ratio, may have a strong prognostic significance in hypertensive and diabetic patients, over and above all other known cardiovascular risk factors. Therefore, regression of vascular alterations is an appealing goal of antihypertensive treatment. Different antihypertensive drugs seem to have different effect on vascular structure. In diabetic hypertensive patients, a significant regression of structural alterations of small resistance arteries with drugs blocking the renin-angiotensin system (angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers) was demonstrated. Alterations in the microcirculation represent a common pathological finding, and microangiopathy is one of the most important mechanisms involved in the development of organ damage as well as of clinical events in patients with diabetes mellitus. Renin-angiotensin system blockade seems to be effective in preventing/regressing alterations in microvascular structure.
Rosei
Enrico Agabiti
EA
Department of Medical and Surgical Sciences, University of Brescia, Clinica Medica, Brescia, Italy.
Rizzoni
Damiano
D
D001158:Arteries / Q000503:physiopathology*; D002318:Cardiovascular Diseases / Q000150:complications / Q000503:physiopathology; D048909:Diabetes Complications / Q000503:physiopathology; D003920:Diabetes Mellitus / Q000503:physiopathology* / Q000628:therapy; D004727:Endothelium / Q000503:physiopathology; D006801:Humans