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ShareScienceDaily (Jan. 4, 2010) — A team of researchers, led by Keiichi Fukuda, at Keio University School of Medicine, Tokyo, Japan, has now determined in rodents how congestive heart failure triggers substantive changes to the nerves that control heart function.
The research appears in the Journal of Clinical Investigation.
Heart function is controlled by both the sympathetic nervous system and the parasympathetic nervous system. In congestive heart failure, increased activation of the sympathetic nervous system causes damage to the heart muscle, a decline in heart function, and potentially lethal abnormal heartbeats.
In the study, failing rat heart muscle cells were found to secrete molecules known as gp130-signaling cytokines that caused sympathetic nerves to change the molecule that they used to communicate from norepinephrine to acetylcholine.
The clinical significance of these observations in rodents was highlighted by the fact that the sympathetic nervous system in the heart of patients with congestive heart failure showed evidence of the same switch to reliance on acetylcholine for communication.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Hideaki Kanazawa, Masaki Ieda, Kensuke Kimura, Takahide Arai, Haruko Kawaguchi-Manabe, Tomohiro Matsuhashi, Jin Endo, Motoaki Sano, Takashi Kawakami, Tokuhiro Kimura, Toshiaki Monkawa, Matsuhiko Hayashi, Akio Iwanami, Hideyuki Okano, Yasunori Okada, Hatsue Ishibashi-Ueda, Satoshi Ogawa and Keiichi Fukuda. Heart failure causes cholinergic transdifferentiation of cardiac sympathetic nerves via gp130-signaling cytokines in rodents. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI39778
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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