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Neuropeptide Y reduces acetylcholine release and vagal bradycardia via a Y2 receptor-mediated, protein kinase C-dependent pathway.

Abstract:

The co-transmitter neuropeptide Y (NPY), released during prolonged cardiac sympathetic nerve stimulation, can attenuate vagal-induced bradycardia. We tested the hypothesis that NPY reduces acetylcholine release, at similar concentrations to which it attenuates vagal bradycardia, via pre-synaptic Y2 receptors modulating a pathway that is dependent on protein kinase A (PKA) or protein kinase C (PKC). The Y2 receptor was immunofluorescently colocalized with choline acetyl-transferase containing ...

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Publication status:
Published

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Publisher copy:
10.1016/j.yjmcc.2007.10.001

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Institution:
University of Oxford
Division:
MSD
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Physiology Anatomy & Genetics
Role:
Author
Journal:
Journal of molecular and cellular cardiology
Volume:
44
Issue:
3
Pages:
477-485
Publication date:
2008-03-01
DOI:
EISSN:
1095-8584
ISSN:
0022-2828
Source identifiers:
105350

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