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Disruption of inhibitory G-proteins mediates a reduction in atrial beta-adrenergic signaling by enhancing eNOS expression.

Abstract:

OBJECTIVE: Cardiac parasympathetic nerve activity is reduced in most cardiovascular disease states, and this may contribute to enhanced cardiac sympathetic responsiveness. Disruption of inhibitory G-proteins (Gi) ablates the cholinergic pathway and increases cardiac endothelial nitric oxide (NO) synthase (eNOS) expression, suggesting that NO may offset the impaired attenuation of beta-adrenergic regulation of supraventricular excitability. To test this, we investigated the role of endogenous ...

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Publication status:
Published

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Institution:
University of Oxford
Department:
Oxford, MSD, RDM, Cardiovascular Medicine, BHF Centre of Research Excellence
Role:
Author
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Journal:
Cardiovascular research
Volume:
67
Issue:
4
Pages:
613-623
Publication date:
2005-09-05
DOI:
EISSN:
1755-3245
ISSN:
0008-6363
URN:
uuid:79f7396c-63a8-4289-84e4-1dbc04305003
Source identifiers:
104969
Local pid:
pubs:104969

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