Journal article
The Ion Channel ASIC2 Is Required for Baroreceptor and Autonomic Control of the Circulation
Neuron (Cambridge, Mass.), Vol.64(6), pp.885-897
12/24/2009
DOI: 10.1016/j.neuron.2009.11.007
PMCID: PMC2807410
PMID: 20064394
Abstract
Arterial baroreceptors provide a neural sensory input that reflexly regulates the autonomic drive of circulation. Our goal was to test the hypothesis that a member of the acid-sensing ion channel (ASIC) subfamily of the DEG/ENaC superfamily is an important determinant of the arterial baroreceptor reflex. We found that aortic baroreceptor neurons in the nodose ganglia and their terminals express ASIC2. Conscious ASIC2 null mice developed hypertension, had exaggerated sympathetic and depressed parasympathetic control of the circulation, and a decreased gain of the baroreflex, all indicative of an impaired baroreceptor reflex. Multiple measures of baroreceptor activity each suggest that mechanosensitivity is diminished in ASIC2 null mice. The results define ASIC2 as an important determinant of autonomic circulatory control and of baroreceptor sensitivity. The genetic disruption of ASIC2 recapitulates the pathological dysautonomia seen in heart failure and hypertension and defines a molecular defect that may be relevant to its development.
Details
- Title: Subtitle
- The Ion Channel ASIC2 Is Required for Baroreceptor and Autonomic Control of the Circulation
- Creators
- Yongjun Lu - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAXiuying Ma - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USARasna Sabharwal - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAVladislav Snitsarev - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USADonald Morgan - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAKamal Rahmouni - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAHeather A Drummond - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USACarol A Whiteis - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAVivian Costa - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAMargaret Price - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAChristopher Benson - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAMichael J Welsh - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAMark W Chapleau - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USAFrançois M Abboud - Department of Internal Medicine and Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242, USA
- Resource Type
- Journal article
- Publication Details
- Neuron (Cambridge, Mass.), Vol.64(6), pp.885-897
- Publisher
- Elsevier Inc
- DOI
- 10.1016/j.neuron.2009.11.007
- PMID
- 20064394
- PMCID
- PMC2807410
- ISSN
- 0896-6273
- eISSN
- 1097-4199
- Language
- English
- Date published
- 12/24/2009
- Academic Unit
- Neurology; Molecular Physiology and Biophysics; Pulmonary, Critical Care, and Occupational Medicine; Critical Care; Iowa Neuroscience Institute; Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology; Neurosurgery; Internal Medicine
- Record Identifier
- 9984020653202771
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