Figure 129

Excess epithelial sodium channel activity in Liddle's syndrome. The epithelial sodium channel responsible for sodium reabsorption in much of the distal portions of the nephron is a complex of three homologous subunits, a, |3, and 7 each with two membrane-spanning domains. Liddle's syndrome, an autosomal dominant disorder causing low renin-aldosterone hypertension often with hypokalemia, results from mutated |3 or 7 subunits. These mutations increase the sodium reabsorptive rate by way of these channels by keeping them open longer, increasing sodium channel density on the membranes, or both. The specific problem appears to reside with proline (P)-rich domains in the carboxyl terminal region of |3 or 7 that are involved in regulation of the channel membrane localization or activity. The net result is excess sodium reabsorption and a reduced capability to increase sodium excretion in response to volume expansion [31,32].

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