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Genetic defects that increase the Cl<jats:sup>\u2212<\/jats:sup>conductance of the junctional complexes may also lead to salt retention and hypertension. Less dramatic alterations in regulatory actions of other hormones such as vasopressin (VP), either alone or with other genetic variations, diet, or environmental factors, may also produce Na<jats:sup>+<\/jats:sup>retention or loss. Although VP acts primarily to regulate water balance, it is also an antinatriuretic hormone. Elevated basal plasma VP levels, and\/or augmented VP release with increased Na<jats:sup>+<\/jats:sup>intake, have been linked to essential hypertension in humans and in animal models of congestive heart failure and cirrhosis. Norepinephrine, dopamine, and prostaglandin E<jats:sub>2<\/jats:sub>can inhibit the antinatriuretic effects of VP, and changes in the actions of these autocrine and paracrine regulators may also be involved in abnormal regulation of Na<jats:sup>+<\/jats:sup>reabsorption.<\/jats:p>","DOI":"10.1152\/ajprenal.00068.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:35:38Z","timestamp":1425414938000},"page":"F221-F235","source":"Crossref","is-referenced-by-count":68,"title":["Abnormal regulation of ENaC: syndromes of salt retention and salt wasting by the collecting duct"],"prefix":"10.1152","volume":"283","author":[{"given":"James A.","family":"Schafer","sequence":"first","affiliation":[{"name":"Departments of Physiology and Biophysics, and Medicine, University of Alabama at Birmingham, Birmingham, Alabama 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