Abstract
Sinoatrial node (SAN) disease mechanisms are poorly understood, and therapeutic options are limited. Natriuretic peptide(s) (NP) are cardioprotective hormones whose effects can be mediated partly by the NP receptor C (NPR-C). We investigated the role of NPR-C in angiotensin II (Ang II)-mediated SAN disease in mice. Ang II caused SAN disease due to impaired electrical activity in SAN myocytes and increased SAN fibrosis. Strikingly, Ang II treatment in NPR-C −/− mice worsened SAN disease, whereas co-treatment of wild-type mice with Ang II and a selective NPR-C agonist (cANF) prevented SAN dysfunction. NPR-C may represent a new target to protect against the development of Ang II-induced SAN disease.
Original language | English |
---|---|
Pages (from-to) | 824-843 |
Number of pages | 20 |
Journal | JACC: Basic to Translational Science |
Volume | 3 |
Issue number | 6 |
DOIs | |
Publication status | Published - Dec 2018 |
Bibliographical note
Funding Information:Supported by Canadian Institutes of Health Research grants MOP 93718 and 142486 to Prof. Rose. Prof. Rose holds a New Investigator Award from the Heart and Stroke Foundation of Canada. Dr. Egom is an employee of ECTRS Ltd. Mr. Mackasey is the recipient of a Libin Cardiovascular Institute of Alberta graduate scholarship. Dr. Egom held a Heart and Stroke Foundation of Canada fellowship. Dr. Jansen holds a Killam postdoctoral fellowship. Dr. Liu is the recipient of a Cumming School of Medicine postdoctoral scholarship. The other authors have reported that they have no industry relationships relevant to the contents of this paper to disclose. Dr. Egom is currently affiliated with the Department of Medicine, St. Martha’s Regional Hospital, Antigonish, Nova Scotia, Canada.
Publisher Copyright:
© 2018 The Authors
ASJC Scopus Subject Areas
- Cardiology and Cardiovascular Medicine