Urinary pCO2 as an index of collecting duct hydrogen ion secretion during chronic hypercapnia

D. C. Batlle, W. Schlueter, R. Foley, N. A. Kurtzman

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

The rise in urinary pCO2 above blood pCO2 which occurs in response to bicarbonate loading (i.e. the urine to blood (U-B) pCO2 gradient), is used with increasing frequency as an index of collecting duct hydrogen ion secretion. We recently proposed, however, that the U-B pCO2 gradient is not an appropriate index of collecting duct hydrogen ion secretion when blood pCO2 is altered acutely. This issue was further investigated by examining the effect of chronic hypercapnia on urinary pCO2 generation. In rats exposed to chronic hypercapnia induced by breathing 10% CO2 for 3 days in an environmental chamber, acute sodium bicarbonate infusion resulted in a U-B pCO2 lower than that of normocapnic control rats (11±4.6 and 30±1.8 mm Hg, p<0.001). This finding could be interpreted to indicate that collecting duct hydrogen ion secretion is depressed in rats with chronic hypercapnia. The urinary pCO2 of rats with chronic hypercapnia was lower than that of the blood (54±6.0 and 86±1.2 mm Hg, p<0.005), respectively). In these rats, NaHCO3 infusion, while blood pCO2 was kept constant, elicited a marked rise in urine pCO2 (from 54±6.0 to 104±6.0 mm Hg, p<0.005) which was not significantly different from that observed in normocapnic control rats. The infusion of carbonic anhydrase resulted in a comparable fall in urine pCO2 in hypercapnic and normocapnic rats (-27±5 and -30±3 mm Hg). In rats with chronic hypercapnia treated with amiloride to inhibit collecting duct H+ secretion, the infusion of NaHCO3 also resulted in a rise in urine pCO2 (from 64±5.6 to 90±4.0 mm Hg, p<0.001). This increment in urine pCO2 (i.e. the ΔpCO2) was lower than that observed in rats with chronic hypercapnia not treated with amiloride (26±5.0 and 50±11 mm Hg, p<0.05) thereby demonstrating that maximal urinary pCO2 generation in rats with chronic hypercapnia requires intact collecting duct H+ secretion. We conclude that in rats with chronic hypercapnia the U-B pCO2 achieved during bicarbonate loading is subnormal owing to the high blood pCO2, and not the result of impaired collecting duct hydrogen ion secretion. The normal rise in urinary pCO2 elicited by sodium bicarbonate loading and the normal fall in urine pCO2 after carbonic anhydrase infusion reflect that collecting duct H+ secretion in rats exposed to chronic hypercapnia is intact. In contrast, colleting duct H+ secretion is clearly underestimated by the U-B pCO2 gradient.

Original languageEnglish (US)
Pages (from-to)230-239
Number of pages10
JournalMineral and Electrolyte Metabolism
Volume11
Issue number4
StatePublished - Jan 1 1985

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry

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