Chloride, renal tubular reabsorption

Elevates osmotic pressure of glomerular filtrate, increases flow of water into interstitial fluid and plasma, inhibiting renal tubular reabsorption of sodium, chloride, producing diuresis. Enhances flow of water from eye into plasma, reducing intraocular pressure (IOP)... 

Sodium and chloride are the major osmotic constituents of glomerular filtrate that need to be conserved by reabsorptive transport across the renal tubular epithelium. Double-barreled Cl -selective liquid ion-exchange microelectrodes were used to measure intracellular Cl concentration in single cellular elements of the proximal tubular epithelium. 

Diuretics increase the rate of urine formation. One common class of diuretics is the thiazide type represented by hydrochlorothiazide. The thiazides affect the renal tubular mechanisms of electrolyte reabsorption and therefore directly increase excretion of sodium and chloride ions. Hypertension has been linked to high sodium ion content and diuretics are used to combat hypertension by decreasing sodium levels. The thiazides... 

As the ascending limb of the loop re-enters the renal cortex, sodium continues to be removed from the tubular fluid by the sodium pump, accompeinied electrostatically by chloride. Both ions pass into the interstitial tissue (site 3) from which they are rapidly removed because cortical blood flow is high and there are no vasa recta present consequently the urine becomes more dilute. Thiazides act principally at this cortical diluting segment of the ascending limb, preventing sodium reabsorption. They inhibit the NaCl co-transporter (called NCCT). 

Oxalate is excreted primarily by the kidney. Oxalate is freely filtered at the glomerulus, where its concentration is normally 1 5 pM. One of the few physiologic functions of oxalate occurs in the proximal tubule where it plays a role in transcellular reabsorption of chloride (mainly present as sodium chloride). Cl entry across the apical membrane is mediated by Cl /oxalate exchange (oxalate is recycled from the tubular lumen to the cell by oxalate/ sulfate exchange, in parallel with Na /sulfate cotransport) [4]. Early studies of renal oxalate clearance using radio-labeled oxalate showed secretion in almost all subjects studied. More recent studies using direct measurement of serum and urine... 

Metabolic compensation occurs when respiratory alkalosis persists for more than 6 to 12 hours. In response to the alkalemia, proximal tubular bicarbonate reabsorption is inhibited and the serum bicarbonate concentration falls. Renal compensation is usually complete within 1 to 2 days. The renal bicarbonaturia, as well as decreased NH4+ and titratable acid excretion, are direct effects of the reduced PaC02 and pH on renal reabsorption of chloride and bicarbonate. The... 

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