Abstract:Serotonin is a vasoactive substance that in different blood vessels mostly induces vasoconstriction. Considering the important role of common carotid artery in brain blood supply, the aims of this study were to investigate the effect of serotonin on isolated rat common carotid artery and also to examine participation of intact endothelium, cyclooxygenase products, Ca++ channels and 5-HT2 receptors in serotonin-evoked action. Endothelium was mechanically removed from some vascular rings. Circular artery segment… Show more
“…This is primarily accomplished by timely and balanced production and release of endothelial relaxing factors, namely, nitric oxide, prostacyclin, or endothelium-derived hyperpolarizing factor [2–4], as well as endothelium-derived contracting autacoids, such as endothelin-1, thromboxane A 2 , angiotensin II, or superoxide anion. The response of different blood vessels to action of various relaxing and contractile vasoactive substances can be partly or entirely endothelium dependent, as well completely endothelium independent [5–8]. Endothelial cells are highly specialized to detect diverse physical, chemical, or mechanical stimuli, such as pulsatile changes in blood flow-induced shear stress, which is pivotal for physiological autoregulation of vascular tone.…”
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.
“…This is primarily accomplished by timely and balanced production and release of endothelial relaxing factors, namely, nitric oxide, prostacyclin, or endothelium-derived hyperpolarizing factor [2–4], as well as endothelium-derived contracting autacoids, such as endothelin-1, thromboxane A 2 , angiotensin II, or superoxide anion. The response of different blood vessels to action of various relaxing and contractile vasoactive substances can be partly or entirely endothelium dependent, as well completely endothelium independent [5–8]. Endothelial cells are highly specialized to detect diverse physical, chemical, or mechanical stimuli, such as pulsatile changes in blood flow-induced shear stress, which is pivotal for physiological autoregulation of vascular tone.…”
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.
“…The calcium-mediated vascular effects of different vasoactive substances in general involve the activation of calcium channels or/and Na + /K + -ATPase [8, 14]. In our experiments we have recorded a strong reduction in bradykinin-induced contraction after the voltage-gated L-type Ca 2+ channels were blocked with nifedipine.…”
Section: Discussionmentioning
confidence: 61%
“…The methodology described in this article was in accordance with our previous investigations [8, 14, 15]. The left and right femoral arteries were carefully isolated from rats, dissected from connective and fat tissue, cut into 4mm–long vascular rings and immediately placed in Krebs-Ringer bicarbonate solution.…”
Bradykinin (BK) plays an important role in different physiological processes including the general preservation and modulation of vascular systems. The present study was designed in order to examine the effect of BK on isolated rat femoral artery rings and to investigate the participation of intact endothelium, cyclooxygenase products, Ca2+ channels, Na+/K+–ATPase, and B2 kinin receptors in BK-induced action. Circular artery segments were placed in organ baths. The endothelium was mechanically removed from some arteries. Concentration–contraction curves for BK were obtained in the rings previously equilibrated at the basal tone. BK produced a concentration–dependent contraction, which was reduced by endothelial denudation. The BK–induced effect was almost completely inhibited by indomethacin (cyclooxygenase inhibitor) or OKY–046 (thromboxane A2–synthase inhibitor). Nifedipine (Ca2+ channel blocker), ouabain (Na+/K+–ATPase inhibitor), or HOE–140 (selective B2 kinin receptor antagonist) significantly reduced the BK–evoked effect. In conclusion, it can be proposed that BK produces concentration– and endothelium–dependent contractions of the isolated rat femoral artery, which is for the most part a consequence of B2 kinin receptor activation. Cyclooxygenase contractile products, especially thromboxane A2, play a significant role in this course of action. The transduction mechanism involved in the process of BK–induced femoral artery contraction include the activation of voltage–gated Ca2+ channels, and in a smaller extent Na+/K+–ATPase as well.
“…In the first part of this study, serotonin produced concentration‐dependent contraction of the isolated rat femoral artery in all groups and subgroups. This was expected because serotonin is well known as a compound that produces contractile effects in the arteries of different animal species . The serotonin‐induced contraction was endothelium‐dependent in the group of healthy animals, but it was independent of the endothelium presence in the rest of the groups/subgroups.…”
Recent findings have demonstrated that serotonin is an important participant in the development and progression of peripheral artery diseases. Taking this into consideration, the goals of this study were to investigate the effects of serotonin on isolated Wistar rat femoral arteries in both healthy and diabetic animals, with and without artery occlusion, with a particular focus on determining the role of calcium in this process. Contraction experiments with serotonin on intact and denuded femoral artery rings, in the presence or absence of nifedipine and ouabain (both separately, or in combination), as well as Ca -free Krebs-Ringer bicarbonate solution were performed. The serotonin-induced results were concentration dependent, but only in healthy animals. The endothelium-dependent contraction of the femoral artery was assessed. In healthy animals, the endothelium-reliant part of contraction was dependent on the extracellular calcium, while the smooth muscle-related part was instead dependent on the intracellular calcium. In diabetic animals, both nifedipine and ouabain influenced serotonin-induced vascular effects by blocking intracellular calcium pathways. However, this was diminished after the simultaneous administration of both blockers.
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