Control of Na+ and Water Absorption Across Vertebrate ‘Tight’ Epithelia By ADH and Aldosterone
Author(s) -
Simon A. Lewis
Publication year - 1983
Publication title -
journal of experimental biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.367
H-Index - 185
eISSN - 1477-9145
pISSN - 0022-0949
DOI - 10.1242/jeb.106.1.9
Subject(s) - aldosterone , apical membrane , vesicle , biophysics , microbiology and biotechnology , membrane , sodium , antidiuretic , cytoplasm , vasopressin , hormone , chemistry , biology , electrolyte , endocrinology , biochemistry , organic chemistry , electrode
Salt and water balance in vertebrates in controlled by the release of two blood borne hormones: aldosterone and antidiuretic (ADH). It is the purpose of this chapter to review the mechanisms (at the plasma membrane level) by which these hormones cause an increase in salt (sodium) and water movement in the target tissues. The primary effect of aldosterone is to increase the Na+ permeability of the lumen-facing (apical) membrane by activation of pre-existing quiescent channels at short times, and by the incorporation of newly synthesized channels after prolonged exposure. Other effects might involve an increase in energy supply and synthesis of Na+-K+ ATPase which is responsible for Na+ extrusion from cell cytoplasm to blood. Similarly, ADH stimulates pre-existing quiescent apical membrane Na+ channels. The second effect of ADH is to increase epithelial water permeability. Evidence strongly suggests that water channels exist in cytoplasmic vesicles which, upon ADH challenge, fuse into the apical membrane causing a rapid increase in apical membrane hydraulic conductivity. The movements of vesicles are dependent on an intact cytoskeleton. Regulation of electrolyte and non-electrolyte transport will be discussed in the light of the above two mechanisms.
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