Physiology Objectives 33
1.
Titratable acid: amount of filtered acid that has been changed from salt to acid
form as it accepts H+ from tubular secretion
2.
Principle buffer in titratable acid formation: phosphate buffer system
3.
Calculate titratable acid formation rate: one millimole of titratable acid = one
millimole of excreted acid = one millimole of new HCO3- formed
4.
Renal secretion of H+, secretion of titratable acid and bicarbonate formation:
The collecting duct accepts a Na+ to turn titratable acid salt into its conjugate
base, and this conjugate base accepts an H+ secreted via either the H+ ATPase or
H+/K+ ATPase countertransporter and is formed by H2CO3 dissociation into H+
and HCO3-.
5.
Processes involved in ammonia excretion and production:
a.
Renal production of ammonia and generation of bicarbonate: produced
by metabolism of glutamate to form 2 NH4+ and 2 HCO3- in the proximal
tubule
b.
Non-ionic diffusion and diffusion trapping: NH3 can readily cross the
luminal membrane to enter the filtrate, and once there, can accept a proton
to make NH4+ which is unable to cross the luminal membrane; this occurs
both in the proximal tubule, and in the collecting duct where NH3 enters
from the interstitium
 Note: NH4+ can also enter the filtrate by taking the place of H+ in the
Na+/H+ exchanger of the proximal tubule
c.
Sites of ammonia production and secretion: produced and secreted in the
proximal tubule
d.
Ammonia recycling: NH4+ is reabsorbed by either paracellular
reabsorption or in place of K+ in the Na+/2Cl-/K+ cotransporter in the
ascending loop of Henle. This NH4+ is picked up by the descending loop
of Henle and is recycled via a countercurrent multiplication mechanism
e.
Adaptation of ammonia production to chronic acid-base disturbances:
ammonia will be produced to excrete acid, so in acidosis, ammonia
production will increase, and in alkalosis, ammonia production will
decrease
6.
K+ influence on acid-base balance: K+ loss (hypokalemia) from tubular cells
causes a replacement by H+ from the interstitium to retain electroneutrality. This
causes an increase in H+ excretion via titratable acid and ammonium with an
increased generation of bicarbonate and thus, causes alkalosis.
7.
Calculate total acid excretion: sum of H+ being eliminated as titratable acid,
buffers, and NH4+
8.
Calculate rate of kidney bicarbonate formation: sum of reabsorption of
HCO3-, excretion of titratable acid, and NH4+
9.
Changes in renal tubular secretion of H+ and its influence on:
a.
Bicarbonate reabsorption: H+ secretion originates from H2CO3
dissociation, and thus, increased H+ secretion causes increased HCO3reabsorption
b.
Total acid excretion: increased H+ secretion will form additional acid and
will increase total acid excretion
c.
Sodium and chloride reabsorption: increased H+ secretion leads to
increased Na+ reabsorption via the Na+/H+ countertransporter; increased
bicarbonate reabsorption in the distal tubule via the bicarbonate/Clcountertransporter causes an influx of Cl- into the distal tubular cells;
however, this Cl- is freely reabsorbed, and Cl- reabsorption increases.
10.
General mechanisms of:
a.
Metabolic acidosis: abnormal retention of non-volatile acids
b.
Metabolic alkalosis: excessive loss of H+ or retention of base
c.
Respiratory acidosis: failure of lungs to excrete CO2
d.
Respiratory alkalosis: hyperventilation and excessive excretion of CO2