NaCl reabsorption, kidney

D.Z. Levine, K.D. Bums, J. Jaffey, and M. Iacovitti, Short-term modulation of distal tubule fluid nitric oxide in vivo by loop NaCl reabsorption. Kidney Int. 65, 184—189 (2004). 

Inhibition of carbonic anhydrase activity profoundly depresses bicarbonate reabsorption in the proximal tubule. At its maximal safely administered dosage, 85% of the bicarbonate reabsorptive capacity of the superficial proximal tubule is inhibited. Some bicarbonate can still be absorbed at other nephron sites by carbonic anhydrase-independent mechanisms, and the overall effect of maximal acetazolamide dosage is about 45% inhibition of whole kidney bicarbonate reabsorption. Nevertheless, carbonic anhydrase inhibition causes significant bicarbonate losses and hyperchloremic metabolic acidosis. Because of this and the fact that HCO3" depletion leads to enhanced NaCl reabsorption by the remainder of the nephron, the diuretic efficacy of acetazolamide decreases significantly with use over several days. 

By blocking active NaCl reabsorption in the TAL, inhibitors of Na+-K+-2C1" symport interfere with a critical step in the mechanism that produces a hypertonic medullary interstitium. Therefore, loop diuretics block the kidney s ability to concentrate urine. Also, since the TAL is part of the diluting segment, inhibitors of the Na+-K+-2C1" symporter markedly impair the kidney s ability to excrete a dilute urine during water diuresis. 

The smallest functional unit of the kidney is the nephron. In the glomerular capillary loops, ultrafiltration of plasma fluid into Bowman s capsule (BC) yields primary urine. In the proximal tubules (pT), approx. 70% of the ultrafiltrate is retrieved by isoosmotic reabsorption of NaCl and water. In the thick portion of the ascending limb of Henle s loop (HL), NaCl is absorbed unaccompanied by water. This is the prerequisite for the hairpin countercurrent mechanism that allows build-up of a very high NaQ concentration in the renal medulla In the distal tubules (dT), NaCl and water are again jointly reabsorbed. At the end of the nephron, this process involves an aldosterone-controlled exchange of Na+ against 1C or H. In the collecting tubule (C), vasopressin (antidiuretic hormone, ADH) increases the epithelial permeability for water, which is drawn into the hyperosmolar milieu of the renal medulla and thus retained in the body. As a result, a concentrated urine enters the renal pelvis. 

In the colon, semifluid material entering from the small bowel is thickened by absorption of water and salts (from about 1000 ml to 150 ml per day). If, owing to the action of an irritant purgative, the colon empties prematurely, an enteral loss of NaCl, KC1 and water will be incurred. In order to forestall depletion of NaCl and water, the body responds with an increased release of aldosterone (p.168), which stimulates their reabsorption in the kidney. However, the action of aldosterone is associated with increased renal excretion of KC1. The enteral and renal K losses add up to K+ depletion of the body, evidenced by a fall in serum K concentration (hypokalemia). This condition is accompanied by a reduction in intestinal peristalsis (bowel atonia). The affected individual infers constipation and again partakes of the purgative, and the vicious circle is closed. 

The most important hormone secreted by the adrenal glands for salt balance is aldosterone. In the absence of this hormone, large quantities of sodium are excreted by the kidney and survival is only possible if a 0.9% NaCl solution is available in place of drinking water. Aldosterone, a steroid hormone acts on the kidney to cause sodium resorption in the distal convoluted tubule, partly in exchange for potassium. Increased sodium reabsorption raises the solute concentration of body fluids. Adrenal hormones in mammals also facilitate the resorption of sodium and chloride from sweat and saliva and also cause increased sodium resorption in the gut. Low sodium ion concentration triggers the secretion of aldosterone. But other body conditions like increased potassium concentration, decreased cardiac output and stress too can induce aldosterone secretion. 

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