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Br J Pharmacol. 2003 Jul;139(5):982-8. doi: 10.1038/sj.bjp.0705329.

Evaluation of potassium ion as the endothelium-derived hyperpolarizing factor (EDHF) in the bovine coronary artery.

British journal of pharmacology

Silvia Nelli, William S Wilson, Hilary Laidlaw, Andrea Llano, Susan Middleton, Andrew G Price, William Martin

Affiliations

  1. Division of Neuroscience & Biomedical Systems, Institute of Biomedical & Life Sciences, West Medical Building, University of Glasgow, Glasgow G12 8QQ, Scotland.

PMID: 12839872 PMCID: PMC1573923 DOI: 10.1038/sj.bjp.0705329

Abstract

1. This study explored the role of the potassium ion in endothelium-derived hyperpolarizing factor (EDHF)-mediated vasodilatation in the bovine coronary artery. 2. Bradykinin-induced, EDHF-mediated vasodilatation was blocked by the Na(+)-K(+) ATPase inhibitor, ouabain (1 micro M), in a time-dependent manner, with maximal blockade seen after 90 min. In contrast, the K(IR) channel inhibitor, Ba(2+) (30 micro M), had no effect. 3. When the potassium content of the bathing solution was increased in a single step from 5.9 to 7-19 mM, powerful vasodilatation (max. 75.9+/-3.6%) was observed. Vasodilatation was transient and, consequently, cumulative addition of potassium produced little vasodilatation, with vasoconstriction predominating at the higher concentrations. 4. The magnitude of potassium-induced vasodilatation was similar in endothelium-containing and endothelium-denuded rings, and was unaffected by Ba(2+) (30 micro M), but abolished by ouabain (1 micro M). 5. Ouabain (1 micro M, 90 min) powerfully blocked bradykinin-induced, nitric oxide-mediated vasodilatation as well as that induced by the nitrovasodilator, glyceryl trinitrate, but that induced by the K(ATP) channel opener, levcromakalim, was hardly affected. 6. Thus, activation of Na(+)-K(+) ATPase is likely to be involved in the vasodilator responses of the bovine coronary artery to both nitric oxide and EDHF. These findings, together with the ability of potassium to induce powerful, ouabain- but not Ba(2+)-sensitive, endothelium-independent vasodilatation, are consistent with this ion contributing to the EDHF response in this tissue.

References

  1. Br J Pharmacol. 1999 May;127(1):27-34 - PubMed
  2. Am J Physiol. 1999 Mar;276(3 Pt 2):H1107-12 - PubMed
  3. J Physiol Pharmacol. 1999 Dec;50(4):525-34 - PubMed
  4. Br J Pharmacol. 2000 Feb;129(4):811-9 - PubMed
  5. Br J Pharmacol. 2000 Aug;130(8):1983-91 - PubMed
  6. Br J Pharmacol. 2000 Nov;131(5):965-73 - PubMed
  7. Br J Pharmacol. 2001 Jan;132(1):293-301 - PubMed
  8. Am J Physiol Heart Circ Physiol. 2001 Mar;280(3):H1113-21 - PubMed
  9. Br J Pharmacol. 2001 Apr;132(7):1558-64 - PubMed
  10. Am J Physiol Heart Circ Physiol. 2001 Jun;280(6):H2413-6 - PubMed
  11. Am J Physiol Heart Circ Physiol. 2001 Jun;280(6):H2424-9 - PubMed
  12. Am J Physiol Heart Circ Physiol. 2001 Jun;280(6):H2441-50 - PubMed
  13. Am J Physiol Heart Circ Physiol. 2001 Jun;280(6):H2478-83 - PubMed
  14. Br J Pharmacol. 2001 Sep;134(1):1-5 - PubMed
  15. Am J Physiol Heart Circ Physiol. 2002 Aug;283(2):H606-14 - PubMed
  16. Circ Res. 1980 Jun;46(6):826-36 - PubMed
  17. Blood Vessels. 1983;20(5):255-64 - PubMed
  18. Eur J Pharmacol. 1985 Apr 2;110(2):203-9 - PubMed
  19. Circ Res. 1985 Jul;57(1):164-70 - PubMed
  20. Am J Physiol. 1994 Mar;266(3 Pt 2):H952-8 - PubMed
  21. Br J Pharmacol. 1995 Oct;116(4):2201-6 - PubMed
  22. Br J Pharmacol. 1996 Apr;117(7):1600-6 - PubMed
  23. J Physiol. 1996 Aug 1;494 ( Pt 3):715-26 - PubMed
  24. J Cardiovasc Pharmacol. 1996 Nov;28(5):703-11 - PubMed
  25. J Physiol. 1996 Apr 15;492 ( Pt 2):419-30 - PubMed
  26. Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):4193-8 - PubMed
  27. Br J Pharmacol. 1997 Sep;122(1):112-6 - PubMed
  28. J Physiol. 1998 Apr 15;508 ( Pt 2):561-73 - PubMed
  29. Nature. 1998 Nov 19;396(6708):269-72 - PubMed
  30. Gen Pharmacol. 1999 Jul;33(1):35-41 - PubMed

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