Open AccessNontubular epithelial Na + channel proteins in cardiovascular regulation
Author(s) -
Drummond Heather A.
Publication year - 2015
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12404
Subject(s) - epithelial sodium channel , reabsorption , endocrinology , medicine , natriuresis , chemistry , microbiology and biotechnology , blood pressure , sodium , kidney , biology , organic chemistry
The role of Epithelial Na+ Channel (ENaC) proteins in cardiovascular regulation and blood pressure control traditionally have been viewed through the lens of ENaC-dependent salt and water transport in the renal cortical collecting duct. In this nephron segment, decreases in ENaC expression/activity lead to salt and water wasting resulting in hypotension and increases lead to hypertension via increased renal salt and water reabsorption. However, the article entitled “Enhanced expression of epithelial sodium channels causes salt-induced hypertension in mice through inhibition of the α2 isoform of Na+, K+ ATPase” in the current issue (Leenen et al. 2015), as well as previous publications from this and other groups, demonstrate that non-tubular ENaC proteins contribute to cardiovascular regulation beyond their direct role in cortical collecting duct salt and water transport (Huang and Leenen 2005; Guan et al. 2009; Wang et al. 2009; Kusche-Vihrog et al. 2010; Drummond 2012).