Stojanović, Marko (56817075100)Marko (56817075100)StojanovićProstran, Milica (7004009031)Milica (7004009031)ProstranRadenković, Miroslav (7005551185)Miroslav (7005551185)Radenković2025-07-022025-07-022019https://doi.org/10.1080/13813455.2018.1437185https://www.scopus.com/inward/record.uri?eid=2-s2.0-85041855732&doi=10.1080%2f13813455.2018.1437185&partnerID=40&md5=c642673463f60fb66689963631111eaahttps://remedy.med.bg.ac.rs/handle/123456789/12838We have performed an in vitro study on isolated intact or denuded femoral artery (FA) of healthy, diabetic, and/or rats submitted to the FA occlusion. The aim was to determine the contribution of endothelium and endothelial dysfunction (ED) on serotonin-induced action in FA. Further, the contribution of angiotensin II and cyclooxygenase products of arachidonic acid was investigated. A marker of ED, vWF was measured in animal serum. Serotonin induced contraction-dependent contraction of isolated FA, which was increased in preparations with endothelium. Pathological conditions such as endothelial denudation, nicotine-induced ED, diabetes or occlusion of FA reduced serotonin-induced contraction. Comparable reduction of serotonin-induced contraction was achieved after inhibition of AT1 receptors with losartan in isolated FA with intact endothelium. Our results demonstrate that angiotensin II contributes to the enhancement of serotonin-induced contraction of femoral arteries with intact endothelium. This increase is attenuated by endothelium removal, nicotine treatment, vascular occlusion, and/or hyperglycemia. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.angiotensin IIdiabetesendothelial dysfunctionSerotoninvascular occlusion