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

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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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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 Caudevilla, 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.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.rights.uri info:eu-repo/semantics/openAccess
dc.source 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.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 info:eu-repo/semantics/article
dc.date.updated 2015-05-08T11:57:06Z
dc.identifier.doi http://dx.doi.org/10.1371/journal.pone.0106372
dc.identifier.idgrec 102400

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