Your browser doesn't support javascript.
loading
A protective role of Nox1/NADPH oxidase in a mouse model with hypoxia-induced bradycardia.
Kojima, Akiteru; Matsumoto, Akio; Nishida, Hirofumi; Reien, Yoshie; Iwata, Kazumi; Shirayama, Takeshi; Yabe-Nishimura, Chihiro; Nakaya, Haruaki.
Afiliação
  • Kojima A; Department of Pharmacology, Chiba University Graduate School of Medicine, Chiba, Japan; Department of Cardiovascular Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
  • Matsumoto A; Department of Pharmacology, Chiba University Graduate School of Medicine, Chiba, Japan.
  • Nishida H; Department of Pharmacology, Chiba University Graduate School of Medicine, Chiba, Japan.
  • Reien Y; Department of Pharmacology, Chiba University Graduate School of Medicine, Chiba, Japan.
  • Iwata K; Department of Pharmacology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
  • Shirayama T; Department of Cardiovascular Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
  • Yabe-Nishimura C; Department of Pharmacology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
  • Nakaya H; Department of Pharmacology, Chiba University Graduate School of Medicine, Chiba, Japan. Electronic address: nakaya@faculty.chiba-u.jp.
J Pharmacol Sci ; 127(3): 370-6, 2015 Mar.
Article em En | MEDLINE | ID: mdl-25837936
ABSTRACT
Although it has been reported that endotoxin-induced expression of Nox1 in the heart contributes to apoptosis in cardiomyocytes, functional role of Nox1 at the physiological expression level has not been elucidated. The aim of this study was to clarify the role of Nox1 under a hypoxic condition using wild-type (WT, Nox1(+/Y)) and Nox1-deficient (Nox1(-/Y)) mice. ECG recordings from anesthetized mice revealed that Nox1(-/Y) mice were more sensitive to hypoxia, resulting in bradycardia, compared to WT mice. Atrial and ventricular electrocardiograms recorded from Langendorff-perfused hearts revealed that hypoxic perfusion more rapidly decreased heart rate in Nox1(-/Y) hearts compared with WT hearts. Sinus node recovery times measured under a hypoxic condition were prolonged more markedly in the Nox1(-/Y) hearts. Sinoatrial node dysfunction of Nox1(-/Y) hearts during hypoxia was ameriolated by the pre-treatment with the Ca(2+) channel blocker nifedipine or the K(+) channel opener pinacidil. Spontaneous action potentials were recorded from enzymatically-isolated sinoatrial node (SAN) cells under a hypoxic condition. There was no significant difference in the elapsed times from the commencement of hypoxia to asystole between WT and Nox1(-/Y) SAN cells. These findings suggest that Nox1 may have a protective effect against hypoxia-induced SAN dysfunction.
Assuntos
Palavras-chave

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Bradicardia / Hipóxia / NADH NADPH Oxirredutases Tipo de estudo: Etiology_studies / Prognostic_studies Limite: Animals Idioma: En Revista: J Pharmacol Sci Assunto da revista: FARMACOLOGIA Ano de publicação: 2015 Tipo de documento: Article País de afiliação: Japão País de publicação: JAPAN / JAPON / JAPÃO / JP

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Bradicardia / Hipóxia / NADH NADPH Oxirredutases Tipo de estudo: Etiology_studies / Prognostic_studies Limite: Animals Idioma: En Revista: J Pharmacol Sci Assunto da revista: FARMACOLOGIA Ano de publicação: 2015 Tipo de documento: Article País de afiliação: Japão País de publicação: JAPAN / JAPON / JAPÃO / JP