Molecular mechanisms of sodium transport inhibition in proximal tubule during acute hypertension.
Acute hypertension provokes a rapid decrease in proximal tubule salt and water reabsorption that increases the levels of sodium chloride at the macula densa, the error signal to increase arteriolar resistance to autoregulate renal blood flow and glomerular filtration rate, and contributes to pressure natriuresis. The molecular mechanisms responsible for this critical homeostatic adjustment are beginning to be dissected: apical sodium transporters in the proximal tubule are redistributed out of the brush border to intermicrovillar and endosomal stores and sodium pump activity is inhibited. These responses are strikingly similar to the cellular responses to parathyroid hormone, and are mediated by similar signalling pathways.
Magyar
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CE
Department of Physiology and Biophysics, USC Keck School of Medicine, Los Angeles, CA 90089, USA.
McDonough
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AA
D000208:Acute Disease; D001485:Basement Membrane / Q000378:metabolism; D002352:Carrier Proteins / Q000378:metabolism; D002908:Chronic Disease; D006801:Humans; D006977:Hypertension, Renal / Q000378:metabolism*; D007687:Kidney Tubules, Proximal / Q000503:physiopathology*; D012964:Sodium / Q000378:metabolism*; D000074083:Sodium-Hydrogen Exchanger 3; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism; D050608:Sodium-Phosphate Cotransporter Proteins; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D027981:Symporters
D002352:Carrier Proteins; D000074083:Sodium-Hydrogen Exchanger 3; D017923:Sodium-Hydrogen Exchangers; D050608:Sodium-Phosphate Cotransporter Proteins; D027981:Symporters; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase