1,721,329 research outputs found
Endothelial Dysfunction in Obesity: Role of Inflammation
No full textEndothelium modulates vascular function and structure, mainly by production of nitric oxide which protects the vasculature against the development of atherosclerosis and thrombosis. Abdominal obesity is associated with vascular endothelial dysfunction, caused by a reduced nitric oxide availability secondary to an enhanced oxidative stress production. Pro-inflammatory cytokine generation is a major mechanism whereby obesity is associated with a reduced NO availability. In healthy conditions, perivascular adipose tissue (PVAT) secretes factors that influence vasodilation by increasing NO availability. Such protective effect is lost in PVAT from obese subjects, which in turn is switched towards a functionally active pro-contractile inflammation source, causing a reduction of vascular NO availability and contributing to the endothelin-1/NO imbalance. In such context, vasculature not only represents a main target of PVAT-derived pro-inflammatory cytokines, but is also considered as important source of low-grade inflammation and oxidative stress which, together with the PVAT, contribute to endothelial dysfunction which characterizes obese patients
Exogenous ghrelin on nitric oxide-endothelin 1 imbalance in metabolic syndrome: can we kill 2 birds with 1 stone?
No full textHow to evaluate microvascular organ damage in hypertension: assessment of endothelial function.
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Use of fixed combination therapies to improve blood pressure control in the clinical management of hypertension: a key opportunity
Full text linkEndothelial Dysfunction in Resistance Arteries of Hypertensive Humans: Old and New Conspirators
No full textA large body of homogeneous reports documented that endothelial dysfunction, which characterizes human essential hypertension is largely dependent on an impaired endothelial nitric oxide availability and an increased production of endothelium-derived contracting factors. These factors include endothelin, prostanoids, and reactive oxygen species (ROS). In particular, it was evidenced that acute intraarterial administration of indomethacin, a nonselective cyclooxygenase (COX)-inhibitor, and ascorbic acid, an antioxidant, normalized the blunted endothelial dysfunction by restoring nitric oxide availability at the level of peripheral microcirculation, thus demonstrating that COX-derived endothelium-derived contracting factors are one of the major sources of ROS. Recent studies put in evidence new lights on the mechanisms involved in endothelial dysfunction in human hypertension, identified as "new conspirators." In particular, functional and immunohistochemical experiments with selective COX inhibitors identified the isoform COX-2 as the main source of intravascular ROS generation in isolated small vessels from essential hypertensive patients. In addition, important vascular protective properties by human ghrelin have been demonstrated in human hypertension, in terms that its systemic reduction is involved in the pathophysiology of endothelial dysfunction, while a normalization of its levels may restore vascular homeostasis
Selective renin inhibition in obese hypertensive patients: perspectives from tissue penetration
No full textLow birth weight and insulin resistance: can capillary recruitment predict hypertension development?
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Does skin microcirculation represent a faithful mirror of uric acid alterations?
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