Acid Base: Renal Regulation Flashcards
key concepts of acid base renal regulation; needed for what, responsible for what, compensation for what
- Buffering and respiratory systems stabilize blood pH……BUT renal function needed for homeostasis (long-term management of pH)
– Responsible for excretion or retention of H+ ions, and fine tuning of extracellular fluid [HCO3-] - Kidneys can adjust excretion of H+ and HCO3- ions as compensation for
– Retention of CO2
– Loss of CO2
– ↑ metabolic production of H + (e.g. ketoacidosis)
– Loss of H+ or HCO3- ions via GIT
renal regulation of HCO3- and H+; contributes to, mechanisms
- Contributes to homeostasis of ECF [H+] by regulating plasma [HCO3- ] and urinary H + excretion
Three mechanisms:
* Altered reabsorption of bicarbonate (essentially “recycling”
* Altered excretion of titratable acid (e.g. HPO42-/HPO4- ).
* Altered excretion of acid in the form of ammonium salts
where does altered bicarb reabsorption mainly happen, what happens when ions increase in blood, savanging
primarily in proximal tubule (70-85% of filtered load)
When H+ ions increase in blood (pH drops), then transport mechanisms for HCO3 - increase. This “scavenges” more bicarbonate for use as buffer
Scavenging doesn’t significantly change in tubular fluid pH (so minimal direct) Immediate change of ECF pH but this“saves” HCO 3 - that will be used as a buffer). Altered Bicarbonate Reabsorption H+
actual secretion of H+ ions, net acid excretion
- In order to actually change the pH of the blood, the body needs to excrete H+ ions and, if possible, generate additional new buffer (HCO3- ).
- Net acid excretion occurs when secreted H+ associates with phosphate (or sulfate) in tubular fluid or whenever NH 4+ is excreted in urine with Cl -
- This effectively leads to the reabsorption of additional (“new”) bicarbonate – “new” because it would otherwise be lost as CO2 when H+ was in excess.
- Distal tubular processes
altered titratable acid excretion in distal nephron; increased expression of Carbonic anhydrase and H+ATPase
Increased expression of Carbonic Anhydrase leads to increased H+ and HCO3 -
Increased H +ATPase and HCO3/Cl- antiporter increases transport of H+ to lumen and HCO3- to blood (increased buffering). Decreased HPO42-/SO42- uptake allows titration and secretion of H+
where does most of the acid secretion happen in distal nephron
Primarily in Distal Tubule & CD - ~33% of Acid Excretion
ammonium excretion; what is NH3 produced from, where does this happen
NH 3 produced in the cortex from
Glutamine
Also Primarily in Distal Tubule & CD - 66 % of Acid Excretion. [H +] can be 1000 X greater in the lumen than in the cell.
intercalated cells; specific cells present where, evolved for what, activity is increased when
Specific cells present in collecting duct and distal tubule. Highly evolved for secretion of H + due to high expression of H+ and H+/K+ ATPase.
Activity is increased in acidosis and decreased in alkalosis.
distal nephron segments determine urine pH; allows what, what does the CD have
- Allows selective excretion or retention of H+ so urine pH can be different from plasma
- Collecting duct has specialized cells that can generate steep H+ concentration gradient
– Intercalated cells
* Rich in carbonic anhydrase
– Alter rate of H + ion secretion by insertion or removal of proton pumps in the apical plasma membrane
– Normally also excrete potassium, but may not do so as efficiently when acidosis is present
factors that stimulate H+ excretion
- Acidosis (metabolic or respiratory)
– ↑ Na +-H + exchange in proximal tubule (increased activity of anti-porters, later synthesis of new exchangers)
– Enhanced ammonium production (increase uptake and metabolism of glutamine)
– Increased H +-ATPase activity in collecting ducts - Hypokalemia
– Shift of H + out of cells, more available for secretion by tubular cells ⇒ H + excreted in exchange for potassium - Aldosterone
– Stimulates luminal H+-ATPase
