La Trobe
1159307_Li,J_2021.pdf (1.78 MB)

Diabetes Attenuates the Contribution of Endogenous Nitric Oxide but Not Nitroxyl to Endothelium Dependent Relaxation of Rat Carotid Arteries

Download (1.78 MB)
journal contribution
posted on 2021-07-28, 03:44 authored by JC Li, A Velagic, CX Qin, M Li, CH Leo, BK Kemp-Harper, Rebecca RitchieRebecca Ritchie, OL Woodman
Endothelial dysfunction is a major risk factor for several of the vascular complications of diabetes, including ischemic stroke. Nitroxyl (HNO), the one electron reduced and protonated form of nitric oxide (NO•), is resistant to scavenging by superoxide, but the role of HNO in diabetes mellitus associated endothelial dysfunction in the carotid artery remains unknown.

Funding

This work was supported in part by the National Health and Medical Research Council (NHMRC) of Australia (to RHR and BKK, APP1120859). Diabetes Australia Research Trust Y13M1-RITR (to RHR and BKK) and the Victorian Government's Operational Infrastructure Support Program. RHR was an NHMRC Senior Research Fellow (APP1059960). QX received a National Heart Foundation Future Leader Fellowship. AV is supported by a Research Training Program (RTP) Scholarship and a Monash Graduate Excellence Scholarship (MGES) provided by Monash University.

History

Publication Date

2021-01-21

Journal

Frontiers in Pharmacology

Volume

11

Article Number

ARTN 585740

Pagination

16p.

Publisher

FRONTIERS MEDIA SA

ISSN

1663-9812

Rights Statement

The Author reserves all moral rights over the deposited text and must be credited if any re-use occurs. Documents deposited in OPAL are the Open Access versions of outputs published elsewhere. Changes resulting from the publishing process may therefore not be reflected in this document. The final published version may be obtained via the publisher’s DOI. Please note that additional copyright and access restrictions may apply to the published version.

Usage metrics

    Journal Articles

    Categories

    No categories selected

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC