Microvascular Responses to Cardiovascular Risk Factors

Department of Molecular & Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130-3932, USA.
Microcirculation (New York, N.Y.: 1994) (Impact Factor: 2.57). 04/2010; 17(3):192-205. DOI: 10.1111/j.1549-8719.2009.00015.x
Source: PubMed


Hypertension, hypercholesterolemia, diabetes, and obesity are among a growing list of conditions that have been designated as major risk factors for cardiovascular disease (CVD). While CVD risk factors are well known to enhance the development of atherosclerotic lesions in large arteries, there is also evidence that the structure and function of microscopic blood vessels can be profoundly altered by these conditions. The diverse responses of the microvasculature to CVD risk factors include oxidative stress, enhanced leukocyte- and platelet-endothelial cell adhesion, impaired endothelial barrier function, altered capillary proliferation, enhanced thrombosis, and vasomotor dysfunction. Emerging evidence indicates that a low-grade systemic inflammatory response that results from risk factor-induced cell activation and cell-cell interactions may underlie the phenotypic changes induced by risk factor exposure. A consequence of the altered microvascular phenotype and systemic inflammatory response is an enhanced vulnerability of tissues to the deleterious effects of secondary oxidative and inflammatory stresses, such as ischemia and reperfusion. Future efforts to develop therapies that prevent the harmful effects of risk factor-induced inflammation should focus on the microcirculation.

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Available from: Daniel Neil Granger, Oct 05, 2015
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    • "Alternatively, cardiovascular risk factors as for example elevated blood cholesterol levels, hypertension, diabetes, obesity and cigarette smoke might directly stimulate microvascular endothelial cell activation with consequent release of inflammatory mediators and soluble isoforms of adhesion molecules, thus determining microvascular dysfunction and the atherosclerosis-associated systemic inflammatory state [11]. In support of this hypothesis, many observations have indicated that the presence of cardiovascular risk factors such as hypercholesterolemia, obesity, hypertension and diabetes induces microvascular responses consistent with the induction of an inflammatory phenotype [12]. In both scenarios, due to its preponderant surface area, microcirculation would quantitatively represent the major source of circulating inflammatory mediators. "
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    IJC Metabolic and Endocrine 06/2014; 3:1–7. DOI:10.1016/j.ijcme.2014.03.002
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    • "Several studies have demonstrated beneficial effects of angiotensin receptor blockers (ARB) on endothelial function, oxidative stress, antioxidant properties, and ventricular remodeling [2]. It was shown that angiotensin II-mediated AT1 receptor stimulation enhances oxidative stress by stimulating NADPH oxidase, with consequent generation of reactive oxygen species [3,4], which, in turn, enhances inactivation of endothelial nitric oxide and accelerates the progression of IRI [5]. Furthermore, AT1 receptors may trigger intracellular reactions contributing to myocyte and vascular hypertrophy, fibrosis, and apoptosis [6]. "
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    04/2014; 20:55-62. DOI:10.12659/MSMBR.890444
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