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American Society for Clinical Investigation Free PMC Article

J Clin Invest. 1988 Sep;82(3):1067-74. doi: 10.1172/JCI113663.

Atrial natriuretic peptides inhibit conductive sodium uptake by rabbit inner medullary collecting duct cells.

The Journal of clinical investigation

M L Zeidel, D Kikeri, P Silva, M Burrowes, B M Brenner

Affiliations

  1. Renal Division, Brigham and Women's Hospital, Boston, Massachusetts 02115.

PMID: 2458385 PMCID: PMC303621 DOI: 10.1172/JCI113663
Free PMC Article

Abstract

The inner medullary collecting duct (IMCD) effects net sodium reabsorption under the control of volume regulatory hormones, including atrial natriuretic peptides (ANP). These studies examined the mechanisms of sodium transport and its regulation by ANP in fresh suspensions of IMCD cells. Sodium uptake was inhibited by amiloride but insensitive to furosemide, bu-metanide, and hydrochlorthiazide. These results are consistent with uptake mediated by a sodium channel or Na+/H+ exchange. To determine the role of sodium channels, cells were hyperpolarized by preincubation in high potassium medium followed by dilution into potassium-free medium. Membrane potential measurements using the cyanine dye, Di(S)-C3-5 verified a striking hyperpolarization of IMCD cells using this protocol. Hyperpolarization increased the apparent initial rate of sodium uptake fourfold. Amiloride and ANP inhibited potential-stimulated sodium uptake 73% and 65%, respectively; the two agents together were not additive. Addition of 5 mM sodium to hyperpolarized cells resulted in a significant amiloride-sensitive depolarization. Half-maximal inhibition of potential-driven sodium uptake occurred at 3 X 10(-7) M amiloride, and 5 X 10(-11) M ANP. We conclude that sodium enters IMCD cells via a conductive, amiloride-sensitive sodium channel, which is regulated by ANP. ANP inhibition of luminal sodium entry in the IMCD appears to contribute to the marked natriuretic effect of this hormone in vivo.

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References

  1. J Membr Biol. 1976 Jun 30;27(4):317-34 - PubMed
  2. Pflugers Arch. 1979 Feb 14;379(1):49-52 - PubMed
  3. Am J Physiol. 1979 Oct;237(4):F247-61 - PubMed
  4. Biochim Biophys Acta. 1980;595(1):15-30 - PubMed
  5. Am J Physiol. 1982 Mar;242(3):C131-45 - PubMed
  6. J Cell Physiol. 1982 Aug;112(2):302-5 - PubMed
  7. Can J Physiol Pharmacol. 1982 Sep;60(9):1149-52 - PubMed
  8. Kidney Int. 1982 Nov;22(5):473-84 - PubMed
  9. Am J Physiol. 1983 Jun;244(6):F666-73 - PubMed
  10. Kidney Int. 1983 May;23(5):711-6 - PubMed
  11. Am J Physiol. 1984 Aug;247(2 Pt 2):F291-302 - PubMed
  12. J Gen Physiol. 1984 Oct;84(4):601-22 - PubMed
  13. Am J Physiol. 1985 Mar;248(3 Pt 1):C241-6 - PubMed
  14. Am J Physiol. 1985 Apr;248(4 Pt 2):F500-6 - PubMed
  15. J Clin Invest. 1986 Jan;77(1):113-20 - PubMed
  16. Biochem Biophys Res Commun. 1986 Jan 29;134(2):852-60 - PubMed
  17. J Clin Invest. 1986 May;77(5):1682-8 - PubMed
  18. Am J Physiol. 1986 Jun;250(6 Pt 2):F963-6 - PubMed
  19. Am J Physiol. 1986 Aug;251(2 Pt 2):F379-83 - PubMed
  20. Am J Physiol. 1986 Dec;251(6 Pt 2):F954-68 - PubMed
  21. J Clin Invest. 1987 Feb;79(2):500-7 - PubMed
  22. Circ Res. 1986 Dec;59(6):605-11 - PubMed
  23. Am J Physiol. 1987 Mar;252(3 Pt 2):F551-9 - PubMed
  24. Miner Electrolyte Metab. 1987;13(1):51-6 - PubMed
  25. Am J Physiol. 1987 Aug;253(2 Pt 1):C177-92 - PubMed
  26. Am J Physiol. 1987 Sep;253(3 Pt 2):F546-54 - PubMed
  27. Am J Physiol. 1987 Oct;253(4 Pt 2):F642-8 - PubMed

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