Relevant bibliographies by topics / Angiotensine II – Antagonistes

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Academic literature on the topic 'Angiotensine II – Antagonistes'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Angiotensine II – Antagonistes"

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Corvol, Pierre, and Pierre-Francois Plouin. "Antagonistes des r??cepteurs de l???angiotensine II." Drugs 62, Special Issue 1 (2002): 53–64. http://dx.doi.org/10.2165/00003495-200262991-00006.

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Turek, Marika, and Piotr Bałczewski. "Pharmaceutical co-crystals of angiotensin II receptor blockers." Chemistry. Environment. Biotechnology 22 (2019): 13–19. http://dx.doi.org/10.16926/cebj.2019.22.02.

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Maillard, Marc P., Catherine Centeno, Åsa Frostell-Karlsson, Hans R. Brunner, and Michel Burnier. "Does protein binding modulate the effect of angiotensin II receptor antagonists?" Journal of the Renin-Angiotensin-Aldosterone System 2, no. 1_suppl (March 2001): S54—S58. http://dx.doi.org/10.1177/14703203010020010901.

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Introduction Angiotensin II AT 1-receptor antagonists are highly bound to plasma proteins (≥ 99%). With some antagonists, such as DuP-532, the protein binding was such that no efficacy of the drug could be demonstrated clinically. Whether protein binding interferes with the efficacy of other antagonists is not known. We have therefore investigated in vitro how plasma proteins may affect the antagonistic effect of different AT1-receptor antagonists. Methods A radio-receptor binding assay was used to analyse the interaction between proteins and the ability of various angiotensin II (Ang II) antagonists to block AT1-receptors. In addition, the Biacore technology, a new technique which enables the real-time monitoring of binding events between two molecules, was used to evaluate the dissociation rate constants of five AT1-receptor antagonists from human serum albumin. Results The in vitro AT 1-antagonistic effects of different Ang II receptor antagonists were differentially affected by the presence of human plasma, with rightward shifts of the IC50 ranging from one to several orders of magnitude. The importance of the shift correlates with the dissociation rate constants of these drugs from albumin. Our experiments also show that the way that AT1-receptor antagonists bind to proteins differs from one compound to another. These results suggest that the interaction with plasma proteins appears to modulate the efficacy of some Ang II antagonists. Conclusion Although the high binding level of Ang II receptor antagonist to plasma proteins appears to be a feature common to this class of compounds, the kinetics and characteristics of this binding is of great importance. With some antagonists, protein binding interferes markedly with their efficacy to block AT1-receptors.
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García-Sáinz, J. A., M. Martínez-Alfaro, M. T. Romero-Avila, and C. González-Espinosa. "Characterization of the AT1 angiotensin II receptor expressed in guinea pig liver." Journal of Endocrinology 154, no. 1 (July 1997): 133–38. http://dx.doi.org/10.1677/joe.0.1540133.

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Abstract In guinea pig hepatocytes angiotensin II induced phosphorylase a activation. This effect was mimicked by other angiotensins with the potency order: angiotensin II (EC50 ≈1 nm)>angiotensin III (EC50 ≈30 nm)>angiotensin I (EC50 ≈300 nm). The effect of 10 nm angiotensin II was blocked by the angiotensin II receptor AT1-selective antagonists irbesartan and losartan (Ki values of ≈1 nm and ≈10 nm for irbesartan and losartan respectively) but not by the AT2-selective antagonist PD123177. Similar data were obtained when the production of [3H]IP3 from [3H]myo-inositol-labeled cells was studied. Angiotensin II induced a dose-dependent increase in [3H]IP3 production; the maximal effect (≈3-fold) was observed at a concentration of 10 μm. This effect of angiotensin II was completely blocked by the AT1-selective antagonists irbesartan and losartan, but only in a very limited fashion by PD123177. [125I][Sar1-Ile8]angiotensin II bound with high affinity (≈3·8 nm) to a moderately abundant number of sites (≈660 fmol/mg protein) in guinea pig liver membranes. Binding competition experiments indicate the following orders of potency for agonists: angiotensin II (≈1·5 nm)>angiotensin III (≈7 nm)>angiotensin I (≈176 nm), and for antagonists: irbesartan (≈0·5 nm)>losartan (≈36 nm)>> PD123177 (>> 10 000 nm). The functional and binding data strongly indicate that the effects of angiotensin II were mediated through AT1 receptors. Expression of the mRNA for these receptors was confirmed by RT-PCR and hybridization of the reaction product with a radiolabeled rat AT1 receptor cDNA probe. Journal of Endocrinology (1997) 154, 133–138
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Nicholls, Kathy. "Angiotensin II antagonists." Nephrology 11 (April 2006): S92—S97. http://dx.doi.org/10.1111/j.1440-1797.2006.00617.x.

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Brunner, Hans R., Jürg Nussberger, Michel Burnier, and Bernard Waeber. "Angiotensin II Antagonists." Clinical and Experimental Hypertension 15, no. 6 (January 1993): 1221–38. http://dx.doi.org/10.3109/10641969309037107.

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Smith, RD, G. Cunningham, and SD Kivlighn. "Angiotensin II antagonists." Emerging Drugs 3, no. 1 (June 1998): 81–94. http://dx.doi.org/10.1517/14728214.3.1.81.

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Mooney, Richard D., Yi Zhang, and Robert W. Rhoades. "Effects of angiotensin II on visual neurons in the superficial laminae of the hamster's superior colliculus." Visual Neuroscience 11, no. 6 (November 1994): 1163–73. http://dx.doi.org/10.1017/s0952523800006969.

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AbstractSuperficial layer superior colliculus (SC) neurons were recorded extracellularly with multibarreled recording/ejecting micropipettes. Angiotensin II was delivered via micropressure ejection during visual stimulation (n = 215 cells), or during electrical stimulation of either the optic chiasm (OX; n = 150 cells) or visual cortex (CTX; n = 42 cells). Application of angiotensin II decreased visual responses of SC cells to 43.8% ± 30.7% (mean ± S.D.) and reduced responses to electrical stimulation of the OX and CTX to 58.6% ± 34.1% and 43.8% ± 30.7% of control values, respectively. Angiotensin II enhanced responses by at least 30% in only 6 cells (1.5%). Of the 35 neurons tested with both OX and CTX stimulation, the correlation of evoked response suppression by angiotensin II was highly significant (r = 0.69; P < 0.001). This suggests that the suppressive effects of angiotensin II were common to both pathways. To test whether the inhibitory effects of angiotensin II were presynaptic or postsynaptic, Mg2+ ions were ejected iontophoretically to abolish synaptic responses, and the neurons were activated by iontophoresis of glutamate and then tested with angiotensin II. Angiotensin II reduced the glutamate-evoked responses to an average 29.1% ± 21.1% of control values (n = 9 cells). This suggests that the site of action of angiotensin II is most likely postsynaptic. To identify which receptors were involved in these effects, angiotensin II was ejected concurrently with the AT1 antagonist Losartan (DUP753) or with either of two AT2 antagonists, CGP42112A or PD123177. Losartan antagonized the action of angiotensin II in 65.6% of the cells tested (n = 99) and CGP42112A and PD123177 had antagonistic effects in 58% (n = 65) and 60% (n = 5), respectively. Both classes of antagonists were tested in 29 cells; and there was no significant correlation between their effectiveness. These results suggest that both AT1, and AT2 receptors may independently mediate the suppressive effects of angiotensin II, and that collicular neurons may have either or both receptor subtypes.
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Baltatu, Ovidiu, Marco A. P. Fontes, Maria J. Campagnole-Santos, Sordaine Caligiorni, Detlev Ganten, Robson A. S. Santos, and Michael Bader. "Alterations of the renin-angiotensin system at the RVLM of transgenic rats with low brain angiotensinogen." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 2 (February 1, 2001): R428—R433. http://dx.doi.org/10.1152/ajpregu.2001.280.2.r428.

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The transgenic rats TGR(ASrAOGEN) (TGR) with low levels of brain angiotensinogen were analyzed for cardiovascular reactivity to microinjections of ANG II and angiotensin receptor (AT1) antagonists [CV-11974, AT1 specific; A-779, ANG-(1–7) selective; sarthran, nonspecific] into the rostral ventrolateral medulla (RVLM) of conscious rats. Microinjection of ANG II resulted in a significantly higher increase in the mean arterial pressure (MAP) of TGR than control [Sprague-Dawley (SD)] rats, suggesting an upregulation of ANG II receptors in TGR. CV-11974 produced an increase in MAP of SD but not in TGR rats. A-779 produced a depressor response in SD but not in TGR rats. Conversely, sarthran produced a similar decrease of MAP in both rat groups. The pressor effect of the AT1 antagonist may indicate an inhibitory role of AT1 receptors in the RVLM. On the other hand, ANG-(1–7) appears to have a tonic excitatory role in this region. The altered response to specific angiotensin antagonists in TGR further supports the functionally relevant decrease in angiotensins in the brains of TGR and corroborates the importance of the central renin-angiotensin system in cardiovascular homeostasis.
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Tatarciuc, Diana, Decebal Vasincu, Gabriela Stoleriu, Roxana Irina Iancu, and Marcel Costuleanu. "Biochemical Effects of Intraliposomal Angiotensins on Isolated Vascular Smooth Muscle Cells." Revista de Chimie 69, no. 5 (June 15, 2018): 1187–90. http://dx.doi.org/10.37358/rc.18.5.6285.

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The intracellular renin-angiotensin effectors (peptides, enzymes, receptors) and their effects are intriguing for a lot of systems. That�s why we aimed the effects of intracellularly-administered angiotensins (angiotensin II, angiotensin III, angiotensin IV, angiotensin fragment 1-7), angiotensinogen, CGP-42112A, apelin, and angiotensin receptors blockers (losartan, PD123319), by the means of liposomes, on apoptosis of cultured isolated rat aortic vascular smooth muscle cells. We evidenced that CGP-42112A (a potent AT2 angiotensin II receptor agonist), administered intracellularly, induced the apoptosis of the cultured isolated vascular smooth muscle cells in a much higher proportion than other agonists and antagonists of angiotensin system: CGP-42112A ] angiotensin II] angiotensin III@ angiotensinogen. Moreover, losartan (an AT1 angiotensin II receptor antagonist), administered intracellularly, induced an important degree of apoptosis of cultured isolated vascular smooth muscle cells. Losartan, administered as concomitant treatment for other angiotensin peptides and CGP-42112A, did not significantly modified the apoptotic effects of these peptides. On the other hand, PD123319 (an AT2 angiotensin II receptor antagonist) was able to significantly reduce the losartan effects when administered as co-treatment for 24 h. The same effects were obtained when LY294002, a PI3K/Akt signaling inhibitor, was administered as a co-treatment. We can conclude an involvement of an AT2 angiotensin II receptor and PI3K/Akt signaling in these apoptotic effects induced by some angiotensin peptides and losartan on cultured isolated rat aortic vascular smooth muscle cells.
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Dissertations / Theses on the topic "Angiotensine II – Antagonistes"

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Estenne, Geneviève. "Conception et synthèse d'antagonistes non-peptidiques de l'angiotensine II." Université Joseph Fourier (Grenoble), 1993. http://www.theses.fr/1993GRE18001.

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Lessinnes, Louis Isabelle. "Antagoniste de l'angiotensine II : place du Telmisartan dans le traitement de l'hypertension artérielle." Paris 5, 2001. http://www.theses.fr/2001PA05P025.

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Maurin, Anne. "Conception, synthèse et évaluation pharmacologique d'antagonistes non peptidiques des récepteurs de l'angiotensine II." Lille 1, 1996. http://www.theses.fr/1996LIL10214.

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La premiere hypothese de travail elaboree pour concevoir une structure originale d'antagonistes non peptidiques des recepteurs de l'ang ii a consiste a copier l'ang ii dans une conformation particuliere, la conformation scorpion. Elle a conduit a la preparation de 4- et 5- (2-alkoxybenzyl)-1-benzylimidazoles et (2-alkoxyphenyl)-(1-benzylimidazol-4 et -5-yl) cetones. Dans un premier temps, des syntheses non regioselectives ont ete envisagees pour la preparation de ces composes. Suite aux difficultes rencontrees lors de la separation des isomeres de position obtenus apres alkylation des synthons (2-alkoxybenzyl)imidazoles, seule la liaison de six derives a pu etre evaluee en binding et aucun ne presente la moindre affinite pour les recepteurs at#1. Le developpement de syntheses regioselectives a permis de surmonter ces difficultes. Trois voies ont ete envisagees et l'une d'entre elle a mene a la preparation du 2-butyl-4-chloro-5-(2-hydroxybenzyl)-1-2'-(1h-tetrazol-5-yl)biphenyl-4-ylmethylimidazole 90. Ce compose n, c benzylimidazole repond a l'hypothese de travail et possede une bonne affinite pour le recepteur at#1(pki = 7,8). D'autre part, l'evaluation pharmacologique de composes issus d'un second concept rationnel qui a pour origine deux antagonistes des recepteurs de l'ang ii, le skf 108566 et le cgp 48933 a ete realisee. Pour cela, une strategie de screening a ete elaboree et differents tests et modeles pharmacologiques ont ete mis au point (binding des recepteurs at#1 et at#2, aorte isolee de lapin, test neurocomportemental d'irwin, modele du rat hypertendu renal). Les meilleurs representants de cette famille possedent des affinites de l'ordre de 10#-#7 m pour les recepteurs at#1. Cinq inhibent la contraction de l'aorte isolee de lapin induite par l'ang ii et trois d'entre eux presentent des effets anihypertenseurs chez le rat hypertendu renal apres administration par voie intraveineuse a la dose de 30mg/kg. Ce travail constitue un point de depart dans les recherches d'antagonistes non peptidiques des recepteurs de l'ang ii. Deux composes chefs de file ont ete obtenus, le derive 90 (pki = 7,8) qui repond a la premiere hypothese de travail et un second (pki = 6,9) qui appartient a la deuxieme famille.
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Sidibé, Aïchata. "Modulation allostérique de l'affinité du récepteur AT1 de l'angiotensine II pour des ligands agonistes et antagonistes." Sherbrooke : Université de Sherbrooke, 1997.

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Meulon, Emmanuelle. "Conception et synthèse de ligands potentiels des récepteurs AT1 et AT2 de l'angiotensine II." Lille 1, 2000. https://pepite-depot.univ-lille.fr/RESTREINT/Th_Num/2000/50376-2000-156.pdf.

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Le système rénine - angiotensine est reconnu aujourd'hui comme l'un des principaux systèmes régulateurs des fonctions cardio-vasculaires et rénales de l'organisme. Par son action vasoconstrictrice puissante, l'angiotensine II joue un rôle fondamental dans la physiopathologie de l'hypertension artérielle. Antagoniser l'angiotensine II, au niveau de son site d'action, constitue le moyen le plus sélectif et le plus efficace de s'opposer à toutes les actions de l'angiotensine II quelles que soient les voies de synthèse de cette hormone. Dans un premier temps, notre travail a consisté à synthétiser des antagonistes sélectifs at 1. Différentes pharmacomodulations ont été réalisées afin d'évaluer l'intérêt de la présence d'une deuxième fonction acide carboxylique, l'importance de la structure 4-methyl-2-yl-1, 1-biphenyle et de la nature de son substituant en 2 sur l'affinité pour le récepteur at 1 de l'angiotensine II. D'autres part, dans le but d'obtenir des ligands mixtes des récepteurs at 1 et at 2, nous avons réalisé différentes modulations au niveau de la structure biphényle et de la nature du substituant (remplacement du tétrazole par un acylsulfonamide ou une sulfonylurée, orientation spatiale de la fonction acide carboxylique par introduction d'un carbonyle entre les deux phényles). L'affinité de ces composés pour le récepteur at 1 a été déterminée par des tests de binding sur des membranes non purifiées de cellules d'hépatome humain (plc-prf-5) et pour le récepteur at 2, sur des membranes non purifiées de cervelet de veau. Les résultats pharmacologiques ont montré, malgré l'introduction d'éléments favorisant la reconnaissance pour le récepteur at 2, la sélectivité de ces molécules pour le récepteur at 1.
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Salfati, Katy. "Effets comparés des inhibiteurs de l'enzyme de conversion et des antagonistes des récepteurs AT1 de l'angiotensine II sur l'insuffisance cardiaque." Paris 5, 2001. http://www.theses.fr/2001PA05P038.

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Foulquier, Sébastien. "Récepteurs AT1-AT2 de l'angiotensine II et propriétés particulières des antagonistes AT1 sur la circulation cérébrale chez le rat." Thesis, Université de Lorraine, 2012. http://www.theses.fr/2012LORR0002.

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Le Système Rénine Angiotensine tient une place prépondérante au sein de la circulation cérébrale. Les Antagonistes des Récepteurs AT1 à l'Angiotensine II (ARAII) ont prouvé leur efficacité dans la prévention de l'Accident Vasculaire Cérébral (AVC), indépendamment de leur effet anti-hypertenseur. Plusieurs mécanismes pourraient être impliqués dans cette cérébroprotection. D'une part, en bloquant les récepteurs AT1, les ARAII favorisent la stimulation des récepteurs AT2 à l'angiotensine II. Le caractère bénéfique lié à la stimulation des récepteurs AT2 s'oppose au caractère délétère lié à la stimulation des récepteurs AT1. Nous avons montré que cet équilibre AT1 - AT2 est modifié au niveau cérébrovasculaire suite à un régime hypersodé. En effet, la vasodilatation des artérioles cérébrales médiée par les récepteurs AT2 est abolie, ce qui pourrait constituer un élément délétère lors de la survenue d'un évènement ischémique. D'autre part, certains ARAII présentent une affinité pour les récepteurs PPAR-gamma. Cette activité, démontrée comme protectrice à différents niveaux vasculaires, pourrait également être bénéfique pour la circulation cérébrale. Nous avons en particulier montré que l'activation PPAR-gamma améliore les effets des ARAII au niveau de la circulation cérébrale (diamètre artériolaire, réactivité à l'angiotensine II). Les mécanismes en jeu semblent impliquer des modifications de la fonction des récepteurs AT1-AT2, indépendamment de leur expression. La stimulation des récepteurs AT2 et l'activation PPAR-gamma constituent donc deux propriétés particulières des ARAII. Ces propriétés pourraient participer au caractère cérébroprotecteur des ARAII, au-delà du seul blocage des récepteurs AT1. Le développement de molécules duales regroupant les activités antagoniste AT1 - agoniste PPAR-gamma pourrait constituer un avenir thérapeutique intéressant dans le traitement de l'hypertension en apportant une protection cérébrovasculaire supérieure aux traitements actuels
The Renin Angiotensin System plays a major role in cerebral circulation. AT1 receptor blockers (ARBs) afford protection against cerebrovascular complications that go beyond that to be expected from their blood pressure lowering action. Several mechanisms could explain such beneficial effects. Firstly, by blocking AT1 receptors, ARBs promote AT2 receptor stimulation by angiotensin II. The beneficial effect related to stimulation of AT2 receptors (vasodilation) counterbalances the deleterious actions of AT1 receptors stimulation. Changes in this ratio may then alter cerebral circulation. We demonstrated that the AT1- AT2 ratio is modified at the cerebrovascular level during high salt intake, which is a risk factor for stroke. The AT2-mediated vasodilation of pial arterioles is abolished. Secondly, some ARBs act as partial agonists of PPAR-gamma. Such an activity, which has been demonstrated to protect extracerebral vessels, could also be beneficial for cerebral circulation. Our results showed that PPAR-gamma activation improves ARB effects on cerebral circulation (arteriolar diameter, angiotensin II reactivity). The underlying mechanisms could imply functional regulation of AT1-AT2 receptors without any change in expression status. AT2 receptor stimulation and PPAR-gamma activity are two special properties of ARBs. These properties could contribute to the cerebroprotection induced by ARBs, beyond the AT1-receptor blockade. Development of new molecules with AT1-receptor blockade and PPAR-gamma activity could take part into the future therapeutic management of hypertension, providing a better cerebrovascular protection
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Foulquier, Sébastien Lartaud Isabelle. "Balance sodée et vasoréactivité cérébrale à l'angiotensine II." [S.l.] : [s.n.], 2008. http://www.scd.uhp-nancy.fr/docnum/SCDPHA_T_2008_FOULQUIER_SEBASTIEN.pdf.

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Prévot, Anne. "Influence de la ciclosporine A sur l'hémodynamique intra-rénale." Dijon, 1999. http://www.theses.fr/1999DIJOMU13.

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La néphrotoxicité chronique de la Ciclosporine A (CsA) a été largement étudiée mais la CsA est de plus en plus fréquemment utilisée pour de courtes périodes. Seulement quelques études ont décrit la néphrotoxicité aiguë et aucune sur le lapin qui présente pourtant de plus grandes similitudes que le rat avec l’humain quant à sa réponse rénale à une exposition chronique à la CsA. Le but de ce travail était de proposer un modèle de néphrotoxicité aiguë de la CsA et d’en étudier les mécanismes. Les expériences ont été réalisées sur des lapins adultes anesthésiés et ventilés mécaniquement. Le débit sanguin rénal et le débit de filtration glomérulaire ont été déterminés par les clairances de l’acide para-aminohippurique et de l’inuline, respectivement. Chaque animal était considéré comme son propre contrôle. Nous avons d’abord rapporté le développement d’un nouveau modèle de néphrotoxicité aiguë de la CsA, d’origine vasomotrice. Cette toxicité n’est pas due au véhicule de la CsA et est partiellement réversible à l’arrêt du traitement. Ce modèle est stable reproductible et nous permet d’étudier les facteurs vasoactifs impliqués. Puis nous avons étudié le rôle des médiateurs potentiellement impliqués dans cette insuffisance rénale en bloquant leur action. L’administration d’un antagoniste des récepteurs de l’endothéline, le bosentan, d’un inhibiteur de l’enzyme de conversion de l’angiotensine, le périndopril, ou d’un antagoniste des récepteurs de l’adénosine, la théophylline, a amélioré l’insuffisance rénale due à la CsA. Enfin, nous avons recherché un effet protecteur de la théophylline, médicament utilisé couramment en clinique humaine. Cet effet n’a pas été retrouvé.
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Grilh, Philippe. "Les antagonistes des récepteurs de l'angiotensine II : pharmacologie comparée avec les inhibiteurs de l'enzyme de conversion." Bordeaux 2, 1997. http://www.theses.fr/1997BOR2P002.

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Books on the topic "Angiotensine II – Antagonistes"

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Philipp, Th, and R. F. Schäfers, eds. Angiotensin II — Antagonismus. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79645-6.

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Parker, James N., and Philip M. Parker. Diovan: A medical dictionary, bibliography, and annotated research guide to internet references. San Diego, CA: ICON Health Publications, 2003.

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Mancia, Giuseppe, ed. Angiotensin II Receptor Antagonists. CRC Press, 2006. http://dx.doi.org/10.1201/9780367804152.

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Mancia, Giuseppe, ed. Angiotensin II Receptor Antagonists. CRC Press, 2006. http://dx.doi.org/10.1201/b14355.

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(Editor), Murray Epstein, and Hans R. Brunner (Editor), eds. Angiotensin II Receptor Antagonists. Hanley & Belfus, 2001.

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Angiotensin II Receptor Antagonists In Perspective. Taylor & Francis, 2000.

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Leyva, F. The Angiotensin II Receptor Antagonists Compendium. Current Medical Literature, 2003.

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Giuseppe, Mancia, ed. Angiotensin II receptor antagonists: Current perspectives. 2nd ed. Abingdon [England]: Informa Healthcare, 2006.

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McInnes, G. T. Pocket Reference to Angiotensin II Antagonists. Science Press, 1997.

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(Editor), Naranjan S. Dhalla, Peter Zahradka (Editor), Ian M.C. Dixon (Editor), and Robert E. Beamish (Editor), eds. Angiotensin II Receptor Blockade: (Progress in Experimental Cardiology). Springer, 1998.

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Book chapters on the topic "Angiotensine II – Antagonistes"

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Timmermans, P. B. M. W. M., and R. D. Smith. "Angiotensin-II-Rezeptoren: Physiologische und pharmakologische Bedeutung." In Angiotensin II — Antagonismus, 1–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79645-6_1.

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Urata, H., S. Hoffmann, H. Nishimura, O. Baltatu, F. Strobel, T. Krause, and D. Ganten. "Mechanismus der Gewebe-Angiotensin-II-Bildung im Herzen und neue Befunde zum kardialen Angiotensin-II-System." In Angiotensin II — Antagonismus, 30–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79645-6_2.

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Dominiak, P., L. Sieroslawski, and H. Brasch. "Wechselwirkungen zwischen Angiotensin II und dem sympathischen System." In Angiotensin II — Antagonismus, 56–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79645-6_3.

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Yeo, W. W., and L. E. Ramsay. "Angiotensin-Konversionsenzym-Inhibitoren, Angiotensin-II-Rezeptor-Antagonisten und persistierender trockener Husten." In Angiotensin II — Antagonismus, 67–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79645-6_4.

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Düsing, R. "Klinische Erfahrungen mit dem Angiotensin-II-Rezeptor-Antagonisten Losartan bei der Behandlung der arteriellen Hypertonie." In Angiotensin II — Antagonismus, 80–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79645-6_5.

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de Gasparo, M. "AT1 Receptor Antagonists: Pharmacology." In Angiotensin Vol. II, 417–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18497-0_18.

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Greenlee, William J., and Ruth R. Wexler. "Medicinal Chemistry of Angiotensin II Antagonists." In Angiotensin Receptors, 67–93. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2464-9_4.

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Maillard, M., and M. Burnier. "Clinical Pharmacology of Angiotensin II Receptor Antagonists." In Angiotensin Vol. II, 453–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18497-0_19.

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Azizi, M., and J. Ménard. "Combined Blockade of the Renin Angiotensin System with ACE Inhibitors and AT1 Receptor Antagonists." In Angiotensin Vol. II, 485–516. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18497-0_20.

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Dendorfer, A., P. Dominiak, and H. Schunkert. "ACE Inhibitors and Angiotensin II Receptor Antagonists." In Atherosclerosis: Diet and Drugs, 407–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27661-0_15.

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Conference papers on the topic "Angiotensine II – Antagonistes"

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Belvisi, Laura, Gianpaolo Bravi, Giovanna Catalano, Massimo Mabilia, and Carlo Scolastico. "Non peptide angiotensin II receptor antagonists: A 3D-QSAR comfa-like approach." In The first European conference on computational chemistry (E.C.C.C.1). AIP, 1995. http://dx.doi.org/10.1063/1.47823.

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Torres, Luis Alberto, Laura Machin, and Seangkin Bum. "Prediction of the Antagonistic Activity On the Receiving AT1 of the Angiotensin II." In MOL2NET 2016, International Conference on Multidisciplinary Sciences, 2nd edition. Basel, Switzerland: MDPI, 2016. http://dx.doi.org/10.3390/mol2net-02-01002.

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Calancea, Valentin, Nelea Ghicavii, Anatol Cretu, Natalia Antonova, Stela Oprea, and Sergiu Matcovschi. "Evaluation in administration of angiotensin II receptor antagonist Valsartan in the treatment of hypertension patients with chronic obstructive pulmonary disease." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2468.

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Hutcheson, Joshua D., Joseph Chen, Larisa M. Ryzhova, and W. David Merryman. "5-HT2B Antagonism Inhibits Strain- and Cytokine-Dependent Formation of Calcific Nodules by Aortic Valve Interstitial Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80496.

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The progression of aortic valve (AV) disease is often characterized by the formation of calcific nodules on thickened AV leaflets, limiting the biomechanical function of the valve. In these cases, the association of extracellular Ca2+ with phosphates remaining in cellular debris within the decellularized scaffolds has been proposed to lead to the nucleation and growth of calcific nodules. In native tissue, calcification is thought to be a more active process involving AV interstitial cells (AVICs). AVICs have been shown to form nodule-like structures in vitro through differentiation to a phenotype with osteogenic character. Additionally, in vitro nodules are characterized by activated smooth muscle α-actin (αSMA) positive AVICs and high levels of apoptosis [1–2]. Mechanical strain has also been shown to influence nodule formation in excised AV leaflets [3]. Our lab has recently developed a model system that recapitulates the formation of calcific nodules in vitro [4]. AVICs treated with TGF-β1 for 24 h prior to the addition of 15% cyclic strain in a Flexcell strain system form nodules that appear to be dependent upon the initiation of AVIC activation. These observations are consistent with previous studies that have shown that αSMA expression is required for nodule formation by AVICs in static culture, with statins shown to inhibit in vitro nodule formation [1]. However, retrospective epidemiological studies have shown that these drugs may not be as effective in preventing calcific valve disease in patients [5]. Additionally, the molecular target and relevant pathways for statins in AVICs remain largely unknown. Therefore, a therapeutically relevant target to prevent AVIC activation and subsequent nodule formation is greatly needed. In this study we investigated the ability of antagonists to 5-HT2B, a receptor known to be upstream of TGF-β1, to oppose strain- and TGF-β1-induced AVIC activation and nodule formation. We also assessed the efficacy of an antagonist to a receptor, the angiotensin II type I receptor (AT1R), known to crosstalk with both 5-HT2B and TGF-β1 signaling in other cell types in inhibiting AVIC nodule formation. Our results indicate that 5-HT2B antagonism inhibits AVIC activation and nodule formation by blocking non-canonical TGF-β1 signaling, whereas AT1R antagonism does not inhibit these outcomes. We believe that the results of this study may indicate novel therapeutic targets to prevent the progression of AV calcification.
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Hermán, F., P. Hadházy, and K. Magyar. "QUANTITATIVE DETERMINATION OF ENDOGENOUS PGI2 RELEASE IN ANAESTHETIZED BEAGLE DOGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643184.

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A 30μm diameter pore size screen was inserted into an arteriovenous bypass system in anaesthetized, heparin-treated beagle dogs. The arterial blood was directed through the screen by a roller pump at a constant rate. As a result, the pressure proximal to the filter continuously increased (F.Hermdn et al.Thromb. Res.44 /1986/,575). The concentration of proximally infused PGI2 that stabilized the filtration pressure curve (pressure stabilizing concentration= PSC) was determined. If it was low enough (between 0.4 and 1.5 nmol/1) we administered the PGI2-releaser bradykinin (1/ug/kg), angiotensin II (0.5/ug/kg) or ADP (20/ug/kg) in bolus dose intravenously. Together with the cnanges in blood pressure, we observed a transient decrease in filtration pressure. From the pressure changes, based on the previously determined PGI2 concentration-res-ponse relationship, we estimated the amounts of released PGI2 as well as the time course of this release. Indomethacin (2 mg/kg i.v.) significantly decreased the PSC for exogenous PGI2 thereby increasing the sensitivity of the method; the release of PGI2 was abolished. The sensitivity of the method could also be increased by infusing BM.13.177 - an endoperoxide, thromboxane receptor antagonist - proximal to the filter (final concentration: 1-10/ug/ml). This substance did not affect the release of PGI2.We conclude that by using this technique the endogenous release of prostacyclin can be continuously determined provided that PGI2 level exceeds 50 pg/ml.
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Reports on the topic "Angiotensine II – Antagonistes"

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Sabit, Zafer, Hristina Nocheva, and Roman Tashev. Modulation of Nociception by Angiotensin II Type 1 Receptors Antagonist Losartan Infused into Amygdala of Rats with a Model of Depression. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, August 2019. http://dx.doi.org/10.7546/crabs.2019.08.15.

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