In the renal tubules: HCO3 А is filtered and then reabsorbed by an interaction

2021-07-26 01:20 PM

This reabsorption is initiated by an in-tubular reaction between the glomerular HCO3- and excreted by the tubular wall cell.

Bicarbonate does not penetrate easily through the renal tubular membrane, so the HCO3- that is filtered out in the glomerulus cannot be reabsorbed directly. Instead, HCO3- is reabsorbed by a special process in which it must first be combined with H + to H2CO3, then dissociated into CO2 and water, as shown in the figure.

Figure. The cytological mechanism of (1) H + secretion into the tubular lumen. (2) The renal tubule reabsorbs HCO3- by combining H + with HCO3- to carbonic acid, then dissociates again into CO2 and water. (3) Na ions, reabsorbed by exchange with the excreted H +. This process occurs in the proximal tubule, the thick segment of the ascending branch of the Henle loop, and the end of the distal tubule.

This reabsorption is initiated by an in-tubular reaction between the glomerular HCO3- and excreted by the tubular wall cell. The H2CO3 produced in this process dissociates immediately into CO2 and water, CO2 can be easily diffused across the tube cell membrane into the tubular cell, where it is reacted with water to form an H2CO3 molecule. new under the catalyst of Carbonic anhydrase. This H2CO3 dissociates into HCO3- and H +, HCO3- diffuses into the intercellular fluid and is carried to the body circulation.

The transport of HCO3- through the cell membrane to the interstitial tissue is done by two mechanisms: (1) Na + -HCO3- channel on the proximal tubule membrane and (2) Cl-HCO3- channel at the end of the proximal tubule. , the thick segment branched onto the loop Henle, and the manifold.

Thus, for each H + formed in the lumen of the renal tubular cell, and HCO3- is also created and released into the bloodstream. The systemic effect of this reaction is the reabsorption of HCO3- from the tubular lumen even though the HCO3- molecule entering the interstitial fluid is not previously filtered HCO3-. This filtrate reabsorption has no effect on the H + reserves of the system because the H + is stored in conjunction with HCO3 А in the dialysis solution, and is therefore not excreted.

HCO3- is "titrated" by H + in the tubular lumen. Under normal conditions, the rate of H + excretion is about 4400 mEq/day, and the filtration rate of HCO3- is about 4320 mEq/day. Thus, the number of these 2 ions entering the kidney tubules is similar, they combine together and form CO2 and water. Therefore, it is said that HCO30 and H + normally "titrate" each other in dialysis solutions.

This "titration" is not always completely accurate because there is often a slight excess of H + (about 80 mEq/day) that degrades the body from the poisoning of metabolic-induced fixed acids. As will be explained later, most of this H + is not excreted as free but is usually in combination with other elements of the urinary buffering system, such as phosphate ions and NH3.

When there is an excess of HCO3 А in urine, as in metabolic alkalosis, this increased amount of HCO3 А cannot be reabsorbed, so this HCO3 А remains in the tubular lumen and excreted in the urine. Helps deal with metabolic alkalosis.

In acidosis, an increase in H + compared to HCO3- increases the reabsorption of HCO3- to the point of complete re-absorption of HCO3-. H + is excreted into the urine as combinations with urine buffers, especially phosphate ions and NH3. Thus, the basic mechanism of the regulation of the acid-base balance of the kidney is due to the incomplete balance between the concentration of H + and HCO3-. Excretion of one of the two ions into urine and removes them from the extracellular fluid.

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