Excretion

Chloride is lost with urine, feces, sweat, and other body secretions. Losses with sweat may be a gram or more per day. While urine always contains at least a small amount (less than 200 mg), renal chloride elimination normally corresponds to recent intakes. Renal excretion: Chloride freely crosses the renal glomerular membrane and about 630 g per day is filtered by the kidneys of a healthy 70 kg male. More than two-thirds of this amount are recovered from the proximal tubular lumen, and nearly 30% from the thick ascending limb (TAD ofthe Hente loop. How much ofthe remainder is absorbed from the distal nephron depends on the homeostatically regulated recovery from distal tubules, connecting segment and collecting tubules.

Both active and passive transport contribute to the movement of chloride out ofthe proximal tubular lumen. Due to its ability to permeate the (not sol tight junctions between proximal tubular epithelial cells, chloride readily diffuses from the highly concentrated luminal fluid directly to the basolateral and pericapillarv space (paraeel-lular transport). At the same time, active transport into the epithelial cell occurs in exchange for formate, fhe basis for this exchange is the fact that non-ionic formate diffuses freely from the lumen into the epithelial cell, where it becomes ionized due to the higher intracellular pi I (established by the apical sodium-hydrogen exchanger 1. NHE3, SLC9A3). The sodium formate exchanger then transports ionized formate back into the lumen while moving chloride into the cell Ultimately, the sodium, potassium-exchanging ATPase (EC3.6,3.0) at the basolateral membrane drives this process by maintaining low intracellular sodium concentration. Pendrin (SLC26A4; the name is derived from Pendred syndrome) explains some ofthe Chloride transport activity, but the principal chloride formate exchanger ofthe proximal tubular brush border membrane remains to be identified (Soleimani, 2001 >, Export across the basolateral membrane into the pericapillary space proceeds via the potassium chloride eotransporters 31KCC3, SLC12A6) and 1 (SLC12A4). As in small intestine, thecAMP-activated ATP-bmding cassette transporter cMOAT MRP2 (ABCC2) regulates chloride efflux across the basolateral membrane I van Kuijck et ul.. 19%).

Tubular chloride in the thin ascending limb ofthe Hcnlc loop uses the chloride channel A to passively follow the concentration gradient ofthe countercurrent system. Reabsorption of sodium chloride in the thick ascending limb of the loop of Hente is active again via the sodium potassium-chloride transporter 2 (NKCC2. SI.C12A I) on the luminal side and chloride channel B on the basolateral side

The thiazidc-sensiiive sodium/chloride cotransporter (SLCI2A3) provides the principal means of chloride reabsorption in the distal nephron (distal tubulus) where the losses are line-tuned in response to chloride status. This transporter is inhibited by thiazide and related diuretics. The potassium chloride cotransporter I (SLCI2A4) completes the transport process on the basolateral side.

Chloride import into the intercalated cells of the cortical collecting duct via pendrin (and the associated secretion of bicarbonate into the tubular lumen) has little relevance for overall chloride reabsorption, but is important for pi I regulation. Perspiration: Chloride constitutes the main anion in sweat at a typical concentration of around 3()mmol L. Sweat production of one liter would thus correspond to a loss

Brush border membrane

Figure tl-6 Reabsorption of chloride from renal tubules n

Capillary lumen

Brush border membrane

Basóla te ral Capillary membra no endothelium

Figure tl-6 Reabsorption of chloride from renal tubules of about one gram. High artibicni temperature, physical exertion, fever, and increased sympathetic activity can induce sweating. Chloride is transported into sweat by the gene product of CLD {SLC26A3).

Understanding And Treating Autism

Understanding And Treating Autism

Whenever a doctor informs the parents that their child is suffering with Autism, the first & foremost question that is thrown over him is - How did it happen? How did my child get this disease? Well, there is no definite answer to what are the exact causes of Autism.

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