By Dale J. Benos (Eds.)
Sodium reabsorbing epithelia play an enormous function in whole-body sodium homeostasis. a few examples of sodium regulating tissues comprise kidney, colon, lung, and sweat ducts. Sodium shipping throughout those membranes is a two-step technique: 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 by way of numerous diversified hormones. The sodium channels additionally play an important position in a couple of sickness 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 pertaining to those sodium channels, their law and involvement in basic and pathophysiological events. Key positive aspects * Summarizes present nation of amiloride-sensitive sodium channel box * Analyzes structure-function of epithelial sodium channels * Discusses immunolocalization of epithelial sodium channels * Examines hormonal legislation of sodium channels * Discusses sodium channels in lymphocytes, kidney, and lung * Considers mechanosensitivity of sodium channels * offers rules on sodium channels and disorder
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Extra resources for Amiloride-Sensitive Sodium Channels: Physiology and Functional Diversity
11). Chang, S. , Mathew, P. ,Lu, Y . , 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).
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.
Hypertension caused by a truncated epithelial sodium channel gamma subunit: Genetic heterogeneity of Liddle syndrome. Nut. Genet. 11,76-82. Hansson, J. , Wilson, T. , Rossier, B. , and Lifton, R. P. (1995b). A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity. Proc. Natl. Acad. Sci. A. 92,11495-11499. Ismailov, I. I.. McDuffie, J. , and Benos, D. J.