食事性NOxの抗メタボ作用と骨髄NOSsの肺保護作用

In this symposium, we introduce our recent studies regarding new actions of diet-derived nitric oxide (NO) and bone marrow-derived NO. A new pathway in which NO is synthesized from NO metabolites; nitrite and nitrate (NOx), is recently discovered. However, whether dietary NOx deficiency causes disea...

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Bibliographic Details
Published in日本薬理学会年会要旨集 p. 3-S21-3
Main Author 筒井, 正人
Format Journal Article
LanguageJapanese
Published 公益社団法人 日本薬理学会 2019
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ISSN2435-4953
DOI10.1254/jpssuppl.92.0_3-S21-3

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Summary:In this symposium, we introduce our recent studies regarding new actions of diet-derived nitric oxide (NO) and bone marrow-derived NO. A new pathway in which NO is synthesized from NO metabolites; nitrite and nitrate (NOx), is recently discovered. However, whether dietary NOx deficiency causes diseases remains to be clarified. We demonstrated that long-term low NOx diet caused metabolic syndrome, vascular dysfunction, and cardiovascular death in mice. These results indicate that dietary NOx plays a pivotal role in the prevention of those disorders (Diabetologia 2017).NO, synthesized by NOSs (nNOS, iNOS, and eNOS), plays a role in the development of pulmonary hypertension. However, the role of NO/NOSs in bone marrow cells in pulmonary hypertension remains elusive. We showed that transplantation of n/i/eNOSs-deficient bone marrow significantly aggravated hypoxia-induced pulmonary hypertension in wild-type mice, and transplantation of wild-type bone marrow significantly ameliorated hypoxia-induced pulmonary hypertension in n/i/eNOSs-deficient mice. These results show that myelocytic n/i/eNOSs play a crucial protective role in the pathogenesis of pulmonary hypertension (Am J Respir Crit Care Med 2018).
Bibliography:92_3-S21-3
ISSN:2435-4953
DOI:10.1254/jpssuppl.92.0_3-S21-3