Altered ENaC Is Associated With Aortic Baroreceptor Dysfunction in Chronic Heart Failure
Author(s) -
Yulong Li,
Dongze Zhang,
Huiyin Tu,
Robert L. Muelleman
Publication year - 2015
Publication title -
american journal of hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.009
H-Index - 136
eISSN - 1941-7225
pISSN - 0895-7061
DOI - 10.1093/ajh/hpv141
Subject(s) - baroreceptor , medicine , epithelial sodium channel , baroreflex , endocrinology , cardiology , heart failure , mechanosensitive channels , aorta , ion channel , blood pressure , heart rate , chemistry , sodium , receptor , organic chemistry
Abnormal baroreceptor function contributes to attenuated arterial baroreflex sensitivity in chronic heart failure (CHF). As a mechanosensor in mammalian nonepithelium, the epithelial sodium channel (ENaC) is an amiloride-sensitive and voltage-independent ion channel. The ENaC is thought to be a component of baroreceptor mechanosensitive ion channels in aortic baroreceptor cell bodies and nerve terminals. In this study, therefore, we measured the expression and activation of the ENaC in nodose neuronal cell bodies and aortic baroreceptor nerve terminals in sham and CHF rats.
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