Skip to main content
PMC home page
The Journal of Clinical Investigation logoLink to The Journal of Clinical Investigation
. 1978 Sep;62(3):532–538. doi: 10.1172/JCI109157

Relationship between the Rate of H+ Transport and Pathways of Glucose Metabolism by Turtle Urinary Bladder

L H Norby 1, John H Schwartz 1
PMCID: PMC371796  PMID: 29052

Abstract

The urinary bladder of the fresh-water turtle acidifies its contents by actively transporting H+ ions across the luminal membrane. It is known that the H+ transport system is dependent upon oxidative metabolism and the substrate glucose; however, the specific biochemical events resulting in H+ translocation have not been identified.

This study examines the relationship between active H+ transport and a specific oxidative pathway of glucose metabolism, the pentose phosphate shunt. To investigate this relationship the metabolic and transport rates were simultaneously measured under several well-defined conditions. When H+ transport was inhibited by either the application of an opposing pH gradient or by acetazolamide, glucose metabolism by the pentose phosphate shunt declined. Conversely, stimulation of H+ transport by either imposing a more favorable pH gradient or by CO2 addition resulted in an increase in pentose phosphate shunt metabolism. Glycolytic activity, in contrast, was invariant with the maneuvers which altered the rate of H+ transport. Additional experiments localized pentose phosphate shunt enzyme activity to the mucosal fraction of the bladder which is the cell layer responsible for acid secretion. The finding that the rate of glucose metabolism by the pentose phosphate shunt is related to the rate of H+ transport suggests but does not prove that the pentose phosphate shunt may be an important metabolic pathway for H+ transport by the turtle urinary bladder.

Full text

PDF
532

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Al-Awqati Q., Beauwens R., Leaf A. Coupling of sodium transport to respiration in the toad bladder. J Membr Biol. 1975 Jun 3;22(1):91–105. doi: 10.1007/BF01868165. [DOI] [PubMed] [Google Scholar]
  2. Al-Awqati Q. Effect of aldosterone on the coupling between H+ transport and glucose oxidation. J Clin Invest. 1977 Dec;60(6):1240–1247. doi: 10.1172/JCI108883. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Al-Awqati Q., Norby L. H., Mueller A., Steinmetz P. R. Characteristics of stimulation of H+ transport by aldosterone in turtle urinary bladder. J Clin Invest. 1976 Aug;58(2):351–358. doi: 10.1172/JCI108479. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Beauwens R., Al-Awqati Q. Active H+ transport in the turtle urinary bladder. Coupling of transport to glucose oxidation. J Gen Physiol. 1976 Oct;68(4):421–439. doi: 10.1085/jgp.68.4.421. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Dies F., Lotspeich W. D. Hexose monophosphate shunt in the kidney during acid-base and electrolyte imbalance. Am J Physiol. 1967 Jan;212(1):61–71. doi: 10.1152/ajplegacy.1967.212.1.61. [DOI] [PubMed] [Google Scholar]
  6. KATZ J., WOOD H. G. The use of C14O2 yields from glucose-1- and -6-C14 for the evaluation of the pathways of glucose metabolism. J Biol Chem. 1963 Feb;238:517–523. [PubMed] [Google Scholar]
  7. Kirchberger M. A., Chen L. C., Sharp G. W. Further studies on the effect of aldosterone on glucose metabolism in toad bladder. Biochim Biophys Acta. 1971 Sep 14;241(3):861–875. doi: 10.1016/0005-2736(71)90014-9. [DOI] [PubMed] [Google Scholar]
  8. Kirchberger M. A., Martin D. G., Leaf A., Sharp G. W. The effect of aldosterone on glucose metabolism in toad bladder. Biochim Biophys Acta. 1968 Aug 6;165(1):22–31. doi: 10.1016/0304-4165(68)90184-0. [DOI] [PubMed] [Google Scholar]
  9. LOWRY O. H., ROSEBROUGH N. J., FARR A. L., RANDALL R. J. Protein measurement with the Folin phenol reagent. J Biol Chem. 1951 Nov;193(1):265–275. [PubMed] [Google Scholar]
  10. MITCHELL P. Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism. Nature. 1961 Jul 8;191:144–148. doi: 10.1038/191144a0. [DOI] [PubMed] [Google Scholar]
  11. Maffly R. H., Edelman I. S. The Coupling of the Short-Circuit Current to Metabolism in the Urinary Bladder of the Toad. J Gen Physiol. 1963 Mar 1;46(4):733–754. doi: 10.1085/jgp.46.4.733. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Nellans H. N., Finn A. L. Oxygen consumption and sodium transport in the toad urinary bladder. Am J Physiol. 1974 Sep;227(3):670–675. doi: 10.1152/ajplegacy.1974.227.3.670. [DOI] [PubMed] [Google Scholar]
  13. Schwartz J. H. H+ current response to CO2 and carbonic anhydrase inhibition in turtle bladder. Am J Physiol. 1976 Aug;231(2):565–572. doi: 10.1152/ajplegacy.1976.231.2.565. [DOI] [PubMed] [Google Scholar]
  14. Schwartz J. H., Rosen S., Steinmetz P. R. Carbonic anhydrase function and the epithelial organization of H+ secretion in turtle urinary bladder. J Clin Invest. 1972 Oct;51(10):2653–2662. doi: 10.1172/JCI107083. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Sernka T. J., Harris J. B. Pentose phosphate shunt and gastric acid secretion in the rat. Am J Physiol. 1972 Jan;222(1):25–32. doi: 10.1152/ajplegacy.1972.222.1.25. [DOI] [PubMed] [Google Scholar]
  16. Spooner P. M., Edelman I. S. Effects of aldosterone on Na+ transport in the toad bladder. I. Glycolysis and lactate production under aerobic conditions. Biochim Biophys Acta. 1976 Oct 22;444(3):653–662. doi: 10.1016/0304-4165(76)90312-3. [DOI] [PubMed] [Google Scholar]
  17. Steinmetz P. R. Acid-base relations in epithelium of turtle bladder: site of active step in acidification and role of metabolic CO2. J Clin Invest. 1969 Jul;48(7):1258–1265. doi: 10.1172/JCI106091. [DOI] [PMC free article] [PubMed] [Google Scholar]
  18. Steinmetz P. R., Omachi R. S., Frazier H. S. Independence of hydrogen ion secretion and transport of other electrolytes in turtle bladder. J Clin Invest. 1967 Oct;46(10):1541–1548. doi: 10.1172/JCI105645. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Journal of Clinical Investigation are provided here courtesy of American Society for Clinical Investigation

RESOURCES