title: Therapeutic approach in the improvement of endothelial dysfunction: the current state of the art.
abstract: The endothelium has a central role in the regulation of blood flow through continuous modulation of vascular tone. This is primarily accomplished by balanced release of endothelial relaxing and contractile factors. The healthy endothelial cells are essential for maintenance of vascular homeostasis involving antioxidant, anti-inflammatory, pro-fibrinolytic, anti-adhesive, or anticoagulant effects. Oppositely, endothelial dysfunction is primarily characterized by impaired regulation of vascular tone as a result of reduced endothelial nitric oxide (NO) synthase activity, lack of cofactors for NO synthesis, attenuated NO release, or increased NO degradation. So far, the pharmacological approach in improving/reversal of endothelial dysfunction was shown to be beneficial in clinical trials that have investigated actions of different cardiovascular drugs. The aim of this paper was to summarize some of the latest clinical findings related to therapeutic possibilities for improving endothelial dysfunction in different pathological conditions. In the majority of presented clinical investigations, the assessment of improvement or reversal of endothelial dysfunction was performed through the flow-mediated dilatation measurement, and in some of those endothelial progenitor cells' count was used for the same purpose. Still, given the fast and continuous development of this field, the evidence acquisition included the MEDLINE data base screening and the selection of articles published between 2010 and 2012.
authors.affiliation: Department of Pharmacology, Clinical Pharmacology and Toxicology, Medical Faculty, University of Belgrade, P.O. Box 38, 11129 Belgrade, Serbia. mradenkovic@med.bg.ac.rs
authors.forename: Miroslav
authors.initials: M
authors.lastname: Radenković
authors.forename: Marko
authors.initials: M
authors.lastname: Stojanović
authors.forename: Tatjana
authors.initials: T
authors.lastname: Potpara
authors.forename: Milica
authors.initials: M
authors.lastname: Prostran
mesh_terms: D002317:Cardiovascular Agents / Q000494:pharmacology; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D009765:Obesity / Q000473:pathology; D011085:Polycystic Ovary Syndrome / Q000473:pathology; D006435:Renal Dialysis; D012307:Risk Factors; D015398:Signal Transduction; D013234:Stem Cells / Q000166:cytology; D014652:Vascular Diseases / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D002317:Cardiovascular Agents; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III