Volatile acid is the product of aerobic cellular respiration, which releases carbon dioxide. As we've learned elsewhere, when carbon dioxide interacts with water in the body fluids, carbonic acid forms.
"Volatile" refers to the fact that carbon dioxide is expired by the lungs.
Non-volatile acids are the products of protein and phospholipid metabolism; they include sulfuric acid and phosphoric acid, and they are excreted in the urine as titratable acids.
Because enzymes and other proteins only function at particular pH values, the body must regulate the acidity of the intra- and extracellular fluids.
Three lines of defense against acid-base imbalance:
In the body, fluids (chemical mixtures), called buffers, minimize pH changes until hydrogen balance can be regained.
The
respiratory system expires carbon dioxide, the source of volatile acid.
The urinary system excretes the non-volatile, aka, fixed, acids.
These systems operate interdependently to maintain an arterial blood plasma pH of 7.4.
Acid Production by Body Tissues
Body tissues produce acids, including carbon dioxide, sulfuric acid, and phosphoric acid; each of these acids releases hydrogen ions that must be buffered in the
body fluid compartments.
Buffering in Fluid Compartments
Intracellular compartment of body tissues = proteins and organic phosphates.
Intracellular compartment of red blood cells =
hemoglobin.
Extracellular fluid = bicarbonate, which is the most important extracellular buffer, and, phosphate and proteins.
When carbonic acid reaches the lungs, it dissociates to form carbon dioxide, which is expired in ventilation.
When pH falls, increased
ventilation triggers to release excess carbon dioxide.
Rapidly, the partial pressure of carbon dioxide drops, and the acidity of the blood is reduced.
In the Kidneys:
Nephrons reabsorb bicarbonate from the filtrate, and excrete hydrogen ions as tritratable acids and ammonium in the urine.
Nearly all of the filtered bicarbonate is reabsorbed from the proximal tubule.
Some hydrogen ions attach to ammonia and are secreted into the filtrate as ammonium; some of this ammonium is then reabsorbed from the thick ascending limb (where it participates in countercurrent multiplication in the renal interstitial fluid).
In the alpha-intercalated cells of the distal nephron, ammonium is again secreted into the tubular fluid, along with phosphoric acid. Phosphoric acid forms when hydrogen ions attach to phosphate, and is often referred to as "titratable acid"
Ammonium and phosphoric acid formation and secretion involve bicarbonate synthesis and reabsorption; this new bicarbonate contributes to the extracellular buffers.
Both mechanisms are responsive to aldosterone, which is a hormone secreted by the
adrenal cortex secreted in response to low pH.
Aldosterone deficiency inhibits ammonium excretion, and causes type 4 renal tubular acidosis. Because potassium excretion is also inhibited by aldosterone deficiency, this type of acidosis is characterized by hyperkalemia.
Alkalosis is a consequence of excessive removal of hydrogen ions from the body fluids; as a result, the blood becomes more alkaline).
Acidosis is the opposite: excessive hydrogen ions are added to the blood or retained; the blood becomes more acidic. Retention of acids can be a sign of renal failure.
