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The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: implications for neural control of cardiac excitability.

Abstract:

The autonomic phenotype of congestive cardiac failure is characterised by high sympathetic drive and impaired vagal tone, which are independent predictors of mortality. We hypothesize that impaired bradycardia to peripheral vagal stimulation following high-level sympathetic drive is due to sympatho-vagal crosstalk by the adrenergic co-transmitters galanin and neuropeptide-Y (NPY). Moreover we hypothesize that galanin acts similarly to NPY by reducing vagal acetylcholine release via a receptor...

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Publication status:
Published
Peer review status:
Peer reviewed
Version:
Publisher's version

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Publisher copy:
10.1016/j.yjmcc.2011.11.016

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Institution:
University of Oxford
Department:
Oxford, MSD
Role:
Author
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Institution:
University of Oxford
Department:
Oxford, MSD, Physiology Anatomy and Genetics
Role:
Author
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Institution:
University of Oxford
Department:
Oxford, MSD, Physiology Anatomy and Genetics
Role:
Author
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British Heart Foundation More from this funder
Academy of Medical Sciences More from this funder
National Institutes of Health More from this funder
Publisher:
Elsevier Publisher's website
Journal:
Journal of molecular and cellular cardiology Journal website
Volume:
52
Issue:
3
Pages:
667-676
Publication date:
2012-03-05
DOI:
EISSN:
1095-8584
ISSN:
0022-2828
URN:
uuid:68d5bd89-edea-44f2-9d96-22218b582891
Source identifiers:
221337
Local pid:
pubs:221337

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