The Ion Channel ASIC2 Is Required for Baroreceptor and Autonomic Control of the Circulation

Yongjun Lu, Xiuying Ma, Rasna Sabharwal, Vladislav Snitsarev, Donald Morgan, Kamal Rahmouni, Heather A. Drummond, Carol A. Whiteis, Vivian Costa, Margaret Price, Christopher Benson, Michael J. Welsh, Mark W. Chapleau, François M. Abboud

Research output: Contribution to journalArticlepeer-review

176 Scopus citations


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.

Original languageEnglish
Pages (from-to)885-897
Number of pages13
Issue number6
StatePublished - 24 Dec 2009




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