By Dale J. Benos (Eds.)
Sodium reabsorbing epithelia play an immense position in whole-body sodium homeostasis. a few examples of sodium regulating tissues contain kidney, colon, lung, and sweat ducts. Sodium delivery 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 shipping and are regulated via numerous diversified hormones. The sodium channels additionally play an important position in a couple of affliction states, like high blood pressure, edema, drug-induced hyperkalemia, and cystic fibrosis. Amiloride-Sensitive Sodium Channels: body structure and sensible range presents the 1st in-depth alternate of rules bearing on those sodium channels, their rules and involvement in basic and pathophysiological occasions. 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 legislation of sodium channels * Discusses sodium channels in lymphocytes, kidney, and lung * Considers mechanosensitivity of sodium channels * presents rules on sodium channels and sickness
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Extra info for Amiloride-Sensitive Sodium Channels: Physiology and Functional Diversity
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. 4A). We took advantage of this to determine the number of y subunits in the channel complex. When we coexpressed equal amounts of wild-type y and yG536C cDNA (with wild-type a and p), the majority of current (77%) was inhibited by MTSET (Fig. 4B). 2), MTSET inhibited 48%of the Na+ current. Thus, MTSET inhibited hENaC out of proportion to the fraction of y subunits that contained the G536C mutation.
1 1 [Amiloride] (FM) FIGURE 8 Amiloride dose-response curves for wild-type, K504E,and K515E abENaC. Although all three channels were sensitive to amiloride, both mutants had much attenuated responses to the diuretic. These data suggest that more than one binding site in abENaC may influence the interaction of the drug with the channel. Reprinted with permission from Fuller ef al. (1997). affected the affinity of the channel for the drug, while excision of the site abolished the amiloride-induced inhibition of the channel.
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). EMBO J. 17, 344-352. Frings, S. , Purves, R. , and MacKnight, A. D. C. (1988). Single channel recordings from the apical membrane of the toad urinary bladder epithelial cell. J. Membr.