Large intestine: Colonocyte

3 Na

Intestinal lumen

Capillary lumen

Brush border membrane

Basolateral Capillary membrane endothelium

Figury 11-î Intestinal sodium absorption sodium mio enterocytes in exchange tor ¿1 proton. Several in the basolateral membrane also mediate sodium influx. Important examples are the sodium/bicarbonate (»transporter iNBCl, SLC4A4, Praetorius el a/.. 2001) and the sodium potassium-chloride transporter ! (SLCI2A2). Both Nlll. and NBC transporters are stimulated by eAMP.

Transport and cellular uptake

Blood circulation: The sodium concentration 111 blood is around 142 mmol/l (3.27 gl). Sodium 111 blood capillaries can get into most tissues simply by diffusing through the gaps between endothelial cells. The gradient between the intracellular sodium concentration (usually around lOmmol Hand the concentration in extracellular fluid drives sodium entry into cells via sodium cotnireporters, sodium hydrogen exchangers (NHE), or sodium channels. Sodium potassium-exchanging ATPase (EC3.6.3.9) pumps sodium against this gradient out of the cell.

Blood brain barrier: Highly effective light junctions in most brain regions block the diffusion of sodium between blood and brain in either direction across the capillary endothelium. This means that sodium flow occurs only through the epithelial cclls via transporters and channels. A few brain regions arc exempted from this tight enclosure, Notably the capillary endothelium adjacent to the vascular organ ofthe lamina terminals in the hypothalamus allows relatively free exchange of sodium. Osmoreceptors in this area sense blood osmolality and thus sodium concentration (Strieker and Svcd, 2000).

Matemo-fetal transfer: Sodium potassium-exchanging ATPase (EC3.6.3.9) at the maternal side maintains the low intracellular sodium concentration of the syntrophoblast layer of the placenta (Johansson et ul., 2000), Since glucose, amino acids and other nutrients and metabolites from maternal blood are transported with sodium into the syntrophoblast. large amounts have to be pumped back again. The same sodium pump is also active at the fetal side, though with less activity. Endogenous digitalis-like factor modulates ATPase activity. In addition to the pumps and cot ran sport ers sodium is moved 111 exchange for protons. The sodium hydrogen exchanger-1 (NHE1. SLCSLC9AI) is located on the maternal side ofthe placental barrier, NIIE3 (SLCSEC9A3) on the fetal side (Pcpe et a!.. 2001). The fetal side also contains a sodium potassium-chloride cotrans porter (Zhao and Hundal. 20(H)).


A 70 kg man contains about iOOg of sodium, about half of that in bone, and 40"« in extracellular fluid.


Sodium is lost mainly with urine and sweat, to a much smaller extent through body secretions, skin, and (less than 0.1 g day) with feces.

Capillary endothelium

Brush border mem bran«

Figure 11,3 Renal handling of sodium

Brush border mem bran«

Capillary endothelium

Capillary lutnen

Figure 11,3 Renal handling of sodium

Renal tosses: Over 600 g day of sodium are filtered into the renal tubules (Kcrailte and Doucet. 211(H). Some of the tillered sodium is taken up from the proximal tubular lumen through the cot rails porters for phosphate, glucose, amino acids, and other substrates. The bulk (about 60%) of filtered sodium is absorbed from the proximal tubular lumen in exchange for protons via the sodium hydrogen exchanger 3 (NHL3. SLC9A3) and to a lesser extent the closely related isoform NHE2 (SLC9A3). Sodium potassium-exchanging ATPase (EC3.6.3.9) is the driving force to pump sodium across the basolateral membrane of the renal epithelial celts (Satoh el a!.. 1999). Additional sodium leaves the thin ascending limb of Henles loop by passive diffusion. The kidney-specific sodium potassium-chloride transporter 2 (SLC12A1. inhibited by the diuretic furosemide) in the thick ascending limb of Denies loop accounts for about 30% of sodium absorption. The distal tubule reabsorbs about 5-7% of the filtered sodium via a sodium chloride transporter (SLC12A3) and basolateral ATPase-mediated transport (Hropot el ul.. 1985). The tinal sodium concentration of urine is adjusted in the distal nephron. Sodium flows into the principal cells of the cortical and medullary collecting tubules through the epithelial sodium channel (LNaC: Su and Menon. 2001) at a rate that is controlled primarily by aldosterone. Excretion with sweat The sodium content of sweat is about 50mmo! I (Shirreffs and Maughan. 1098; Sanders el ul.. 1999). An hour of \ igorous exercise at normal room temperature (22- -25°C) typically induces the loss of about 0.51 sweat, and thus about 0,6g sodium. Exertion near or above body temperature increases sweat production to several liters per day with correspondingly high electrolyte losses. Ingestion ofwater and sugar promote sweating I Kritzsche ei a I., 20(H)). Sympathetic activity increases sweating.

Cholecystokinin. corticotrophin-releasing hormone, enterostatin, leptin, and alpha-melanocyte stimulating hormone (MSH) increase sympathetic activ ity: neuropeptide V. beta-endorphin, orexin. galanin. and melanin concentrating hormone reduce it (Bray. 2000).



Is there a cause or cure for autism? The Complete Guide To Finally Understanding Autism. Do you have an autistic child or know someone who has autism? Do you understand the special needs of an autistic person?

Get My Free Ebook

Post a comment