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Lecture 20

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University of Toronto Scarborough
Biological Sciences
Stephen Reid

1    Lecture 20: Acid-Base Balance 1. Acid-Base Regulation in the Proximal Tubule during Acidosis + In the event of an acidosis, thekidney will increase excretion of H ions and increase the reabsorption of bicarbonate (or possible synthesise new bicarbonate). Within the proximal tubule filtered HCO reacts 3- + with secreted H ions to form H O and C2 (this is ca2alyzed by carbonic anhydrase). The CO diffuses 2 from the tubular fluid into the epithelial cells, where it is hydrated back into HCO - and H (aga3n, via + + - carbonic anhydrase). The H is secreted back into the tubules, whilst the HCO is reabs3rbed (in co-transport with Na or in exchange for a Cl ion). Thus, the acidosis is countered by an increased - + retention of HCO ions3 whilst excess H ions are excreted in the urine (in the form of water). In the event of an alkalosis, bicarbonate reabsorption and proton secretion would be reduced. 2. Acid-Base Regulation in the Distal Tubule during Acidosis This process involves the synthesis of HCO . Once fl3id reaches the distal tubule almost all of the bicarbonate has already been reabsorbed by the proximal tubule and therefore there is little or no bicarbonate to reabsorb. In the epithelial cells of the distal tubule, there are four main exchange mechanisms that will be key to the synthesis of HCO 3-. On the apical membrane (on the inside of the tubule), there are H pumps and H /K antiporters. On the basolateral membrane there are Cl and - - - HCO /C3 antiporters. 2    + - CO 2 diffuses into the tubular epithelial cells from the peritubular fluidand is hydrated into H and HCO 3 ions by carbonic anhydrase. The proton is then secreted, via the H pumps or the H /K antiporter, into + - the tubular lumen, where it is eventually excreted as urine. The HCO is absorbed b3ck into the peritubular fluid via the HCO /Cl a3tiporter, and the Cl ions are simply recycled between the + - peritubular fluid and the tubular cell via a chloride channel. Therefore, overall, H is secreted and HCO 3 is absorbed. Once in the tubular fluid, the H + ions are buffered by HPO in the fluid, and ultimately - 4 excreted in the urine as H PO 2 4 3. Acid-Base Regulation in the Proximal Tubule during a Severe Acidosis During an extremely severe acidosis, a second mechanism becomes activated in the proximal tubules in order to restore acid-base balance. This process also involves synthesizing bicarbonate, but this time from the amino acid, glutamine. It is freely filtered by the glomerulus, and is found in the tubular fluid and quickly absorbed by the tubular epithelial cells. It can also move into the tubular cells from the peritubular fluid. Inside the cells, glutamine is converted to HCO -, NH (ammonia), and an H ion. The + + 3 3 NH 3 combines with the H to form NH (ammonium4 and is secreted back into the fluid and eventually excreted, whilst the bicarbonate ion is moved into the peritubular fluid via Na +/HCO co-transport or - - 3 + Cl /HCO ant3port. The net effect is the same as the other mechanisms for excreting H ions, and - absorbing HCO . 3 3    4. Davenport Diagrams and the Henderson-Hasselbach Equation It is possible to graph and visualise acid-base disturbances on Davenport diagrams pH-bicarbonate ( diagrams). These diagrams plot blood bicarbonate levels (y-axis) against blood pH (or plasma bicarbonate versus plasma pH). Theslope of the relationship between bicarbonate levels and pH is called the buffer line. Blood CO leve2s are also represented by a series ofCO isobars. The2partial pressure of CO (2CO ) is2constant along any given isobar. On this graph the standard starting (normal) levels are a - [HCO ] 3f 25 mM, a pH of 7.4 and a pCO of 40 mmHg.2 Davenport diagrams are a graphical representation of the Henderson-Hasselbach equation. In this equation, α is the solubility coefficient for CO disso2ved in blood. - pH = pK + log [HCO ] /  3CO 2 The buffer line for whole blood is steeper than the buffer line for plasmaindicating that whole blood is a better buffer than is plasma. This isillustrated if you add or remove base (i.e., raise or lower bicarbonate levels) and look at the resulting change in pH. For any change in bicarbonate levels, the pH change in whole blood is less than the pH change in plasma. This is because whole blood has a higher buffering capacity due to the presence of haemoglobin in the red blood cells. 4    5. Primary Acid-Base Disturbances NOTE: It is important to look at the lecture slides as these changes are much more easily visualised than they are to read about. Looking atall of the diagrams is key to understanding these disturbances and the compensation that arises. Acid-base disturbances can be classified in two ways: 1) By the change in pH. If pH goes down it is an acidosis; if pH goes up it is an alkalosis. 2) By the nature of the disturbance. If pCO ch2nges then it is arespiratory disturbance (acidosis or alkalosis). If pCO does 2 not change then it is a metabolic disturbance. A respiratory acid-base disturbance manifests as a movement along the buffer line from one pCO isobar to a2other pCO
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