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Diminished neurogenic femoral artery vasoconstrictor response in a Zucker obese rat model: differential regulation of NOS and COX derivatives

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Diminished neurogenic femoral artery vasoconstrictor response in a Zucker obese rat model: differential regulation of NOS and COX derivatives

dc.contributor.author	Martínez, Ana Cristina
dc.contributor.author	Hernández, Medardo
dc.contributor.author	Novella del Campo, Susana
dc.contributor.author	Martínez, María Pilar
dc.contributor.author	Pagán, Rosa María
dc.contributor.author	Hermenegildo, Carlos
dc.contributor.author	García Sacristán, Albino
dc.contributor.author	Prieto, Dolores
dc.contributor.author	Benedito, Sara
dc.date.accessioned	2015-05-08T11:57:06Z
dc.date.available	2015-05-08T11:57:06Z
dc.date.issued	2014
dc.identifier.citation	Martínez, Ana Cristina Hernández, Medardo Novella, Susana Martínez, María Pilar Pagán, Rosa María Hermenegildo, Carlos García Sacristán, Albino Prieto, Dolores Benedito, Sara 2014 Diminished neurogenic femoral artery vasoconstrictor response in a Zucker obese rat model: differential regulation of NOS and COX derivatives Plos One 9 e106372
dc.identifier.uri	http://hdl.handle.net/10550/43624
dc.description.abstract	Objective: Peripheral arterial disease is one of the macrovascular complications of type 2 diabetes mellitus. This study addresses femoral artery regulation in a prediabetic model of obese Zucker rats (OZR) by examining cross-talk between endothelial and neural factors. Methods and Results: Arterial preparations from lean (LZR) and OZR were subjected to electrical field stimulation (EFS) on basal tone. Nitric oxide synthase (NOS) and cyclooxygenase (COX) isoform expression patterns were determined by immunohistochemical labelling and Western blotting. Results indicate significantly reduced noradrenergic contractions in preparations from OZR compared with those of LZR. Functional inhibition of endothelial NOS (eNOS) indicated a predominant role of this isoform in LZR and its modified activity in OZR. Neural (nNOS) and inducible NOS (iNOS) were activated and their expression was higher in femoral arteries from OZR. Neurotransmission modulated by largeconductance Ca2+-activated (BKCa) or voltage-dependent (KV) K+ channels did not seem compromised in the obese animals. Endothelial COX-1 and COX-2 were expressed in LZR and an additional adventitial location of COX-2 was also observed in OZR, explaining the higher COX-2 protein levels detected in this group. Prostanoids derived from both isoforms helped maintain vasoconstriction in LZR while in OZR only COX-2 was active. Superoxide anion inhibition reduced contractions in endothelium-intact arteries from OZR. Conclusions: Endothelial dysfunction led to reduced neurogenic vasoconstriction in femoral arteries from OZR. In a setting of obesity, NO-dependent nNOS and iNOS dilation activity could be an alternative mechanism to offset COX-2- and reactive oxygen species-mediated vasoconstriction, along with impaired endothelial NO relaxation.
dc.language.iso	eng
dc.relation.ispartof	Plos One, 2014, vol. 9, p. e106372
dc.subject	Fisiologia humana
dc.subject	Diabetis
dc.subject	Medicina
dc.title	Diminished neurogenic femoral artery vasoconstrictor response in a Zucker obese rat model: differential regulation of NOS and COX derivatives
dc.type	journal article	es_ES
dc.date.updated	2015-05-08T11:57:06Z
dc.identifier.doi	10.1371/journal.pone.0106372
dc.identifier.idgrec	102400
dc.rights.accessRights	open access	es_ES