NAGIOS: RODERIC FUNCIONANDO

Complete blockade of the vasorelaxant effects of Ang-(1-7) and bradykinin in murine microvessels by antagonists of the receptor Mas.

Repositori DSpace/Manakin

IMPORTANT: Aquest repositori està en una versió antiga des del 3/12/2023. La nova instal.lació está en https://roderic.uv.es/

Complete blockade of the vasorelaxant effects of Ang-(1-7) and bradykinin in murine microvessels by antagonists of the receptor Mas.

dc.contributor.author	Peiró, Concepción
dc.contributor.author	Vallejo, Susana
dc.contributor.author	Gembardt, Florian
dc.contributor.author	Palacios, Erika
dc.contributor.author	Novella, Susana
dc.contributor.author	Azcutia, Verónica
dc.contributor.author	Rodríguez-Mañas, Leocadio
dc.contributor.author	Hermenegildo, Carlos
dc.contributor.author	Sánchez-Ferrer, Carlos F.
dc.contributor.author	Walther, THOMAS
dc.date.accessioned	2020-09-29T19:03:09Z
dc.date.available	2020-09-29T19:03:09Z
dc.date.issued	2013
dc.identifier.citation	Peiró, Concepción Vallejo, Susana Gembardt, Florian Palacios, Erika Novella, Susana Azcutia, Verónica Rodríguez-Mañas, Leocadio Hermenegildo, Carlos Sánchez-Ferrer, Carlos F. Walther, THOMAS 2013 Complete blockade of the vasorelaxant effects of Ang-(1-7) and bradykinin in murine microvessels by antagonists of the receptor Mas. Journal of Physiology-London 591 9 2275 2285
dc.identifier.uri	https://hdl.handle.net/10550/75691
dc.description.abstract	The heptapeptide angiotensin-(1-7) is a biologically active metabolite of angiotensin II, the predominant peptide of the renin-angiotensin system. Recently, we have shown that the receptor Mas is associated with angiotensin-(1-7)-induced signalling and mediates, at least in part, the vasodilatory properties of angiotensin-(1-7). However, it remained controversial whether an additional receptor could account for angiotensin-(1-7)-induced vasorelaxation. Here, we used two different angiotensin-(1-7) antagonists, A779 and d-Pro-angiotensin-(1-7), to address this question and also to study their influence on the vasodilatation induced by bradykinin. Isolated mesenteric microvessels from both wild-type and Mas-deficient C57Bl/6 mice were precontracted with noradrenaline, and vascular reactivity to angiotensin-(1-7) and bradykinin was subsequently studied using a small-vessel myograph. Furthermore, mechanisms for Mas effects were investigated in primary human umbilical vein endothelial cells. Both angiotensin-(1-7) and bradykinin triggered a concentration-dependent vasodilatation in wild-type microvessels, which was absent in the presence of a nitric oxide synthase inhibitor. In these vessels, the pre-incubation with the Mas antagonists A779 or d-Pro-angiotensin-(1-7) totally abolished the vasodilatory capacity of both angiotensin-(1-7) and bradykinin, which was nitric oxide mediated. Accordingly, Mas-deficient microvessels lacked the capacity to relax in response to either angiotensin-(1-7) or bradykinin. Pre-incubation of human umbilical vein endothelial cells with A779 prevented bradykinin-mediated NO generation and NO synthase phosphorylation at serine 1177. The angiotensin-(1-7) antagonists A779 and d-Pro-angiotensin-(1-7) equally block Mas, which completely controls the angiotensin-(1-7)-induced vasodilatation in mesenteric microvessels. Importantly, Mas also appears to be a critical player in NO-mediated vasodilatation induced by renin-angiotensin system-independent agonists by altering phosphorylation of NO synthase.
dc.language.iso	eng
dc.relation.ispartof	Journal of Physiology-London, 2013, vol. 591, num. 9, p. 2275-2285
dc.subject	Farmàcia Investigació
dc.subject	Fisiologia
dc.title	Complete blockade of the vasorelaxant effects of Ang-(1-7) and bradykinin in murine microvessels by antagonists of the receptor Mas.
dc.type	journal article	es_ES
dc.date.updated	2020-09-29T19:03:09Z
dc.identifier.doi	10.1113/jphysiol.2013.251413
dc.identifier.idgrec	084862
dc.rights.accessRights	open access	es_ES