4.5 Article

A protective role of Nox1/NADPH oxidase in a mouse model with hypoxia-induced bradycardia

期刊

JOURNAL OF PHARMACOLOGICAL SCIENCES
卷 127, 期 3, 页码 370-376

出版社

JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1016/j.jphs.2015.02.007

关键词

NADPH oxidase; Sinoatrial node; Hypoxia

资金

  1. Ministry of Education, Culture, Sports, Science and Technology of Japan [23390053]
  2. Grants-in-Aid for Scientific Research [23390053, 26670119] Funding Source: KAKEN

向作者/读者索取更多资源

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 pretreatment with the Ca2+ 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. (C) 2015 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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