The nature of the renal adaptation to chronic hypocapnia.
Metabolic balance studies were carried out in normal dogs to define the renal mechanisms responsible for the adaptation to, and recovery from, chronic hypocapnia. A chronic reduction in arterial CO(2) tension (Pa(CO2)) of some 15 mm Hg was achieved by means of chronic exposure of the animals to 9% oxygen in an environmental chamber. The development of hypocapnia was associated with a marked suppression of net acid excretion which, together with a slight accumulation of organic acids, produced a reduction in plasma bicarbonate concentration (8 mEq/liter) that led to nearly full protection of extracellular pH (DeltaH(+) = - 2.5 nmoles/liter). When Pa(CO2) was returned to control levels, an augmentation of acid excretion restored plasma composition to normal after a brief period of "posthypocapneic metabolic acidosis."The changes in renal acid excretion during both adaptation and recovery were accomplished in a fashion notably different from that previously observed in chronic hypercapnia, being linked to changes in cation rather than chloride excretion. Thus, in dogs ingesting a normal NaCl diet, suppression of hydrogen ion excretion during adaptation to hypocapnia was associated with an increased excretion of sodium rather than with a retention of chloride. The fact that this loss of sodium occurred without a concomitant loss of potassium strongly suggests that the hypocapneic state specifically depressed distal sodium reabsorption; if distal sodium reabsorption had not been depressed, a reduction in proximal sodium reabsorption or a diminution in distal hydrogen ion secretion (or both) should have produced an increase in potassium excretion. The interpretation that chronic hypocapnia diminished sodium reabsorption was supported by the finding that when renal sodium avidity was enhanced by restriction of sodium intake, acid retention was accomplished by a loss of potassium rather than of sodium. The accompanying reduction in plasma bicarbonate concentration was slightly less than that observed in dogs ingesting a normal NaCl diet, a finding probably accounted for by a slight difference in the availability of cation for excretion under the two experimental circumstances. These findings, taken together with the observation that augmented acid excretion during recovery from hypocapnia is linked to cation retention, suggest that an adequate intake of cation during both adaptation and recovery from chronic hypocapnia may be critical to the physiologic regulation of acid-base equilibrium.
D000042:Absorption; D000136:Acid-Base Equilibrium; D000143:Acids / Q000652:urine; D000222:Adaptation, Physiological; D000818:Animals; D001639:Bicarbonates / Q000097:blood; D001769:Blood; D002245:Carbon Dioxide / Q000097:blood*; D002712:Chlorides / Q000652:urine; D002908:Chronic Disease; D004032:Diet; D004285:Dogs; D005260:Female; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000097:blood; D007668:Kidney / Q000503:physiopathology*; D007684:Kidney Tubules / Q000503:physiopathology; D009318:Natriuresis; D011188:Potassium / Q000652:urine; D012965:Sodium Chloride
D000143:Acids; D001639:Bicarbonates; D002712:Chlorides; D002245:Carbon Dioxide; D012965:Sodium Chloride; D011188:Potassium