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Sci Rep. 2017 Dec 14;7(1):17564. doi: 10.1038/s41598-017-17690-7.

Altered heart rate regulation by the autonomic nervous system in mice lacking natriuretic peptide receptor C (NPR-C).

Author information

1
Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia, Canada.
2
Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia, Canada. robert.rose@ucalgary.ca.
3
School of Biomedical Engineering, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada. robert.rose@ucalgary.ca.
4
Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada. robert.rose@ucalgary.ca.

Abstract

Natriuretic peptides (NPs) play essential roles in the regulation of cardiovascular function. NP effects are mediated by receptors known as NPR-A, NPR-B or NPR-C. NPs have potent effects on regulation of heart rate (HR) by the autonomic nervous system (ANS), but the role of NPR-C in these effects has not been investigated. Accordingly, we have used telemetric ECG recordings in awake, freely moving wildtype and NPR-C knockout (NPR-C-/-) mice and performed heart rate variability (HRV) analysis to assess alterations in sympatho-vagal balance on the heart following loss of NPR-C. Our novel data demonstrate that NPR-C-/- mice are characterized by elevations in HR, reductions in circadian changes in HR and enhanced occurrence of sinus pauses, indicating increased arrhythmogenesis and a loss of HRV. Time domain and frequency domain analyses further demonstrate that HRV is reduced in NPR-C-/- mice in association with a reduction in parasympathetic activity. Importantly, the low frequency to high frequency ratio was increased in NPR-C-/- mice indicating that sympathetic activity is also enhanced. These changes in autonomic regulation were confirmed using atropine and propranolol to antagonize the ANS. These findings illustrate that loss of NPR-C reduces HRV due to perturbations in the regulation of the heart by the ANS.

PMID:
29242602
PMCID:
PMC5730580
DOI:
10.1038/s41598-017-17690-7
[Indexed for MEDLINE]
Free PMC Article

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