Open AccessA novel variant of the beta-subunit of the amiloride-sensitive sodium channel in African Americans.
Author(s) -
Yan Su,
Mark Rutkowski,
Charles Klanke,
Xiaodong Wu,
Yong Cui,
R.Y.K. Pun,
V. Carter,
Max C. Reif,
Anil G. Me
Publication year - 1996
Publication title -
journal of the american society of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.451
H-Index - 279
eISSN - 1533-3450
pISSN - 1046-6673
DOI - 10.1681/asn.v7122543
Subject(s) - amiloride , sodium channel , endocrinology , sodium , epithelial sodium channel , medicine , renal sodium reabsorption , reabsorption , chemistry , basal (medicine) , threonine , methionine , patch clamp , conductance , amino acid , biology , biochemistry , kidney , electrophysiology , phosphorylation , serine , insulin , organic chemistry , mathematics , combinatorics
The amiloride-sensitive sodium channel is responsible for the rate-limiting step of sodium reabsorption in the distal renal tubule, and thus may play a key role in the maintenance of sodium balance and blood pressure. In this study, a genetic variant that results in a change of threonine to methionine at amino acid 594 (T594 M) in the carboxy-terminus of the beta-subunit of the amiloride-sensitive sodium channel has been identified. This variant was present in 6.1% of African-American subjects (N = 231) but was not seen in Caucasians (N = 192). Whole cell voltage clamp of B-lymphocytes from individuals with the T594 M variant showed similar basal membrane slope conductance, compared with the wild-type but increased response to cAMP analog.
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