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Concept

Vasodilatateur

vignette|Le vaisseau sanguin vasodilaté (à droite) laisse passer plus de sang que le vaisseau sanguin normal (à gauche). Un vasodilatateur (contraire de vasoconstricteur) est une substance qui permet de dilater les vaisseaux sanguins, c'est-à-dire d'augmenter leur lumière, en relâchant les muscles lisses des parois de ces vaisseaux. La conséquence principale est la diminution de la pression artérielle car il y a plus de place disponible au sang pour circuler. Par ailleurs, les vasodilatateurs augmentent le débit sanguin du territoire où ils provoquent une vasodilatation. Ils peuvent agir spécifiquement sur certains vaisseaux :

artères, artérioles ;
veines ; ou sur certains territoires.

Ils agissent :

soit par une action directe sur les vaisseaux ;
soit en inhibant une substance vasoconstrictrice.

Plusieurs vasodilatateurs sont utilisés comme médicaments. Ils sont utilisés pour :

baisser la pression artérielle dans le traitement de l'hypertension artérielle ;
améliorer

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Résumé

artères, artérioles ;
veines ; ou sur certains territoires.

Ils agissent :

soit par une action directe sur les vaisseaux ;
soit en inhibant une substance vasoconstrictrice.

Plusieurs vasodilatateurs sont utilisés comme médicaments. Ils sont utilisés pour :

baisser la pression artérielle dans le traitement de l'hypertension artérielle ;
améliorer

Source officielle

À propos de ce résultat

Publications associées (9)

Publications associées

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Personnes associées (1)

Personnes associées

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Unités associées (1)

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Concepts associés (103)

Concepts associés

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Cours associés (4)

Cours associés

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p-Aminobenzamidine attenuates cardiovascular dysfunctions in spontaneously hypertensive rats

Allancer Divino De Carvalho Nunes, Fabiana Pereira Da Costa Fraga, Nikolaos Stergiopulos

Aims:Diminazene aceturate, a putative ACE2 activator, is susceptible to cleavage resulting in the formation of paminobenzamidine (PAB). This study aimed to investigate the effects of PAB in addressing cardiovascular dysfunctions in spontaneously hypertensive rats (SHR). Main methods:Acute effects of PAB on mean arterial pressure (MAP), heart rate (HR), and aortic (AVC) and mesenteric vascular conductance (MVC) were evaluated in anesthetized SHR. Isolated aortic rings and the Langendorff technique were used to investigate the acute and chronic effects of PAB in the artery and heart. Chronic treatment with PAB (1 mg/kg, gavage) was carried out for 60 days. During this period, systolic blood pressure (SBP) and HR were measured by tail-cuff plethysmography. After the treatment, the left ventricle was collected for histology analyses, western blotting, and ACE2 activity. Key findings:Bolus infusion of PAB acutely reduced MAP and increased both AVC and MVC in SHR. Additionally, PAB induced coronary and aorta vasodilation in isolated organs from Wistar and SHR in an endothelialdependent manner. The chronic PAB treatment in SHR significantly attenuated the increase of SBP and improved the aorta vasorelaxation induced by acetylcholine and bradykinin-induced coronary vasodilation. In addition, chronic treatment with PAB attenuated the cardiomyocyte hypertrophy and extracellular matrix deposition in hearts from SHR. PAB did not alter the protein expression of the AT1, AT2, Mas, ACE, ACE2, or ACE2 activity. Significance:PAB induced beneficial effects on cardiovascular dysfunctions induced by hypertension, suggesting that this molecule could be used in the development of new drugs for the treatment of cardiovascular diseases.

PERGAMON-ELSEVIER SCIENCE LTD2022

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Effect of intimal shear and cyclic strech on arterial segments perfused in vitro

Veronica Gambillara

Hemodynamics have crucial role in the control of vascular tone, in the regulation of arterial remodeling, and in the production of mediators that maintain arterial function. Changes in hemodynamics forces induce profound alterations in vascular cell metabolism and function, in the extracellular matrix, and in smooth muscle cell (SMC) phenotypes, all being part of vessel wall remodeling. Vessel wall remodeling plays a key role in arterial wall homeostasis but also in the initiation and development of arterial disease. This aim of this work is to study the effects of two distinct biomechanical stimuli, oscillatory shear and cyclic stretch on vessel wall function. Our 71 investigation is performed using an improved in vitro artery perfusion system, which allows to study the exact contribution of each biomechanical stimulus on isolated arterial segments, where the biological cell responses of endothelial and SMCs, and the extracellular matrix interactions are well preserved. The present thesis is divided into two main sections. The first part focuses on the effects of oscillatory shear stress on arterial segments, a mechanism presumed to be involved in the localization and initiation of atherosclerotic plaques. The second section investigates the influence of reduced cyclic stretch on the arterial wall, a procedure that is occurring in arterial stiffening. In the first and second papers, we examined the effects of three different shear stress conditions on the endothelium, SMC, and arterial wall responses, in porcine carotid arteries perfused in vitro for three days. We demonstrated that oscillatory shear stress, which is usually present in plaque-prone areas, decreased the bradykinin-induced vasorelaxation after 3 days of perfusion. The endothelial dysfunction was correlated to an impaired endothelial nitric oxide synthase gene expression and bradykinin-mediated activation. The potential lack of nitric oxide production and/or bioavailability observed in arteries exposed to oscillatory shear stress may also be the cause of the start of matrix turnover. Expression and activation of matrix metalloproteinase-2 and-9 were increased in arteries exposed to oscillatory shear, suggesting that this type of shear stress triggers a remodeling process. This part of the study provides a new insights on the role of shear stress in the control of arterial function and supports the hypothesis that oscillatory shear stress is a determining factor predisposing the arterial wall to atherosclerosis. The third paper focuses on the effects of cyclic stretch on vascular smooth muscle function, phenotype and wall remodeling. Arteries were wrapped by an external banding, which drastically decreased compliance and therefore the cyclic stretch. Arteries were perfused for one day under a unidirectional shear stress (6±3 dyn/cm2) in combination with a mean pressure of 80 mmHg and a pulse pressure of +/-10 mmHg. We demonstrated that exposure to reduced cyclic stretch induced a rapid modulation of SMC phenotype which was combined with a decrease in norepinephrine-induced vasocontraction. SMC dedifferentiation was associated to a decrease of plasminogen activator inhibitor-1 expression, which, combined with enhanced matrix metalloproteinase-2, may promote wall remodeling and SMC migration. These findings give a further approach into possible consequences of an arterial stiffening on large vessel wall patho-physiology.

EPFL2005

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Role of ERK1/2 activation and nNOS uncoupling on endothelial dysfunction induced by lysophosphatidylcholine

Luciano Dos Santos Aggum Capettini, Nikolaos Stergiopulos

Background and aims: Lysophosphatidylcholine (LPC) - a main component of oxidized LDL -is involved in endothelial dysfunction that precedes atherosclerosis, with an increased superoxide anions and a reduced NO production via endothelial NO synthase (eNOS) uncoupling. However, there is no evidence about the mechanisms involved in neuronal NOS (nNOS) uncoupling. Extracellular signal-regulated kinase (ERK) is related to the control of NO production and inflammatory gene transcription activation in atherosclerosis. Our aim was to investigate the role of nNOS/ERK1/2 pathway on endothelial dysfunction induced by LPC, in mouse aorta and human endothelial cells. Methods: Thoracic aorta from wild type mice was used to perform vascular reactivity studies in the presence or absence of LPC. Human endothelial cells were used to investigate the effect of LPC on expression of nNOS and his products NO and H2O2. Results: LPC reduced acetylcholine (ACh)-induced vasodilation in mouse aorta (Emax(CT/LPC) = similar to 95 +/- 2/ 62 +/- 3%, p = 0.0004) and increased phenylephrine-induced vasoconstriction (Emax(CT/LPC) = similar to 4 +/- 0,1/ 6 +/- 0,1 mN/mm, p = 0.0002), with a reduction in NO (fluorescence intensity(CT/LPC) = 91 +/- 3/62 +/- 2 x 10(3), p = 0.0002) and H2O2 (fluorescence intensityCT/LPC = similar to 16 +/- 0,8/10 +/- 0,7 x 10(3), p = 0.0041) production evocated by ACh. An inhibition of nNOS by TRIM (Emax(CT/CT+TRIM) = similar to 93 +/- 1/43 +/- 3%, p = 0,0048; Emax(LPC/LPC+TRIM) = similar to 62 +/- 3/65 +/- 3%) or H2O2 degradation by catalase (Emax(CT/CT+cat) = similar to 93 +/- 1/46 +/- 2%, p < 0,001; Emax(LPC/LPC+cat) = similar to 62,8 +/- 3,2/60,5 +/- 4,7%) reduced the relaxation in the control but not in LPC group. PD98059, an ERK1/2 inhibitor, abolished the increase in vasoconstriction in LPC-treated vessels (Emax(LPC/LPC+PD) = similar to 6 +/- 0,1/3 +/- 0,1 mN/mm, p = 0.0001). LPC also reduced the dimer/monomer proportion and increased nNOS(ser852) phosphorylation. Conclusions: LPC induced nNOS uncoupling and nNOS(Ser852) phosphorylation, reduced NO and H2O2 production and improved superoxide production by modulating ERK1/2 activity in human and murine endothelial cells. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

Elsevier2017

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Insuffisance cardiaque chez l'humain

L’insuffisance cardiaque (IC) ou défaillance cardiaque correspond à un état dans lequel une anomalie de la fonction cardiaque est responsable de l'incapacité du myocarde à assurer un débit cardiaque

Neurotransmetteur

Les neurotransmetteurs, ou neuromédiateurs, sont des composés chimiques libérés par les neurones (et parfois par les cellules gliales) agissant sur d'autres neurones, appelés neurones postsynaptiques,

Blood pressure

Blood pressure (BP) is the pressure of circulating blood against the walls of blood vessels. Most of this pressure results from the heart pumping blood through the circulatory system. When used withou

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