By Dale J. Benos (Eds.)
Sodium reabsorbing epithelia play a tremendous position in whole-body sodium homeostasis. a few examples of sodium regulating tissues contain kidney, colon, lung, and sweat ducts. Sodium shipping throughout those membranes is a two-step approach: access via an amiloride-sensitive sodium channel and go out through the ouabain-sensitive sodium/potassium ATPase. The sodium access channels are the rate-limiting determinant for delivery and are regulated through numerous various hormones. The sodium channels additionally play an important function in a couple of illness states, like high blood pressure, edema, drug-induced hyperkalemia, and cystic fibrosis. Amiloride-Sensitive Sodium Channels: body structure and useful variety presents the 1st in-depth trade of principles referring to those sodium channels, their law and involvement in general and pathophysiological events. Key beneficial properties * Summarizes present nation of amiloride-sensitive sodium channel box * Analyzes structure-function of epithelial sodium channels * Discusses immunolocalization of epithelial sodium channels * Examines hormonal rules of sodium channels * Discusses sodium channels in lymphocytes, kidney, and lung * Considers mechanosensitivity of sodium channels * presents principles on sodium channels and sickness
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Extra resources for Amiloride-Sensitive Sodium Channels: Physiology and Functional Diversity
W. (1990). Restoration of inactivation in mutants of Shaker potassium channels by a peptide derived from ShB. Science 250, 568-571. CHAPTER 2 Membrane Topology,Subunit Composition, and Stoichiometry of the Epithelial NaS Channel Peter M. Snyder,” Chun Cheng,? and Michael J. Welsh? Departments of Internal Medicine and Physiology and Biophysics, Howard Hughes Medical Institute, University of Iowa College of Medicine, Iowa City, Iowa 52242 I. Introduction 11. Topology of ENaC 111. Subunit Composition of hENaC IV.
Electrophysiologid Analysis The finding that coexpression of a,p, and yENaC is required for maximal Na+ current suggests that ENaC is a heteromultimeric channel. Genetic evidence from C. elegans suggests that the degenerins also function as heteromultimers (Tavernarakis and Driscoll, 1997). , 1998). , 1997) previously found that a residue within the second transmembrane lines the channel pore. Wild-type hENaC is segment of yhENaC insensitive to the cysteine-reactive compound MTSET (Fig. 4A). However, when Gly536was replaced by cysteine (yG536C), MTSET irreversibly inhibited hENaC (87%, Fig.
Shimkets, R. , Rossier, B. , and Lifton, R. P. (1996). Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type I. Nut. Genet. 12, 248-253. 22 C. Fuller et al. , and Chalfie, M. (1991). The mec-4 gene is a member of a family of Caenorhabditis elegans genes that can mutate to induce neuronal degeneration. Nature (London) 349, 588-593. , Merillat, A. , Rossier, B. , and Schild, L. (1998). The heterotetrameric architecture of the epithelial sodium channel (ENaC).