Figure 2. Molecular Mechanisms Mediating Salt Reabsorption in the Kidney and Associated Monogenic Hypertensive Diseases.

The kidney filters more than 180 liters of plasma (containing 23 moles of salt) daily and reabsorbs more than 99 percent of the filtered sodium. The proximal tubule of the nephron reabsorbs about 60 percent of the filtered sodium, primarily by sodium–hydrogen ion exchange. The thick ascending loop of Henle absorbs about 30 percent by sodium–potassium–chloride (Na⁺–K⁺–2Cl^–) cotransporters. The distal convoluted tubule reabsorbs about 7 percent by sodium–chloride cotransporters, and the remaining 3 percent of the filtered sodium is handled by epithelial sodium channels in the cortical collecting tubule. The renin–angiotensin system tightly regulates the activity of the epithelial sodium channels. Decreased delivery of sodium to the loop of Henle leads to renin secretion by the juxtaglomerular apparatus of the kidney. Renin acts on the circulating precursor angiotensinogen to generate angiotensin I, which is converted in the lungs to angiotensin II by angiotensin-converting enzyme. Angiotensin II binds to its specific receptor in the adrenal glomerulosa, stimulating aldosterone secretion. Aldosterone binds to its receptor in the distal nephron, leading to increased activity of the epithelial sodium channels and sodium reabsorption. Monogenetic diseases that alter blood pressure are shown in yellow. (Adapted from Lifton et al.,¹¹ with the permission of the publisher.)

Return to Article

Add to Personal Archive

PowerPoint Help