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Departments of Physiology and Biophysics, and Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294
Although the aldosterone-responsive
segments of the nephron together reabsorb <10% of the filtered
Na+, certain single-gene defects that affect the epithelial
Na+ channel (ENaC) in the luminal membrane of the
collecting duct (CD) or its regulation by aldosterone cause severe
hypertension, whereas others cause salt wasting and hypotension. These
rare defects illustrate the key role of the distal nephron in
maintaining normal extracellular volume and blood pressure. Genetic
defects that increase the Cl
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+
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+
intake, have been linked to essential hypertension in humans and in
animal models of congestive heart failure and cirrhosis. Norepinephrine, dopamine, and prostaglandin E2 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+ reabsorption.
cortical collecting duct; medullary collecting duct; distal convoluted tubule; sodium balance; potassium balance; vasopressin; aldosterone; gene defects; hypertension; sodium transport; potassium transport; chloride transport; epithelial sodium channel
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