Display options
Share it on

Cardiovasc Drugs Ther. 1991 Dec;5(6):1035-41. doi: 10.1007/BF00143532.

The effects of calcium antagonists on extracellular potassium accumulation during global ischaemia in isolated perfused rat hearts.

Cardiovascular drugs and therapy

J B Heijnis, R Coronel, P A van Zwieten

Affiliations

  1. Department of Pharmacotherapy, University of Amsterdam, The Netherlands.

PMID: 1801890 DOI: 10.1007/BF00143532

Abstract

The effects of equipotent concentrations of diltiazem, verapamil, and nifedipine upon the accumulation of extracellular potassium [K+]out and the left ventricular pressure (LVP) were studied during global ischemia in isolated perfused rat hearts. Measurement of [K+]out and LVP were performed in two series of experiments. Diltiazem (2 x 10(-6), 3 x 10(-6), and 10(-5) M), verapamil (3 x 10(-8), 10(-7), and 3 x 10(-7) M), and nifedipine (3 x 10(-8), 10(-7), and 1.5 x 10(-7) M) were able to slow, in a concentration-dependent manner, the initial rate of rise of [K+]out without affecting the final plateau value of [K+]out reached at t = 5 to t = 10 minutes. Notably, at the lowest concentrations, which slightly influenced LVP diltiazem, verapamil, and to a lesser degree nifedipine, were still able to slow the rise in [K+]out. In addition, after preperfusion with low-calcium media [( Ca2+] from 1.8 to 1.3 or 0.9 mM), inducing similar negative inotropic effects as those of the calcium antagonists, the rise in [K+]out was not significantly influenced. Our data indicate that the ability to slow the rise in [K+]out is a specific characteristic of calcium antagonists that is independent of their negative inotropic effects.

References

  1. Basic Res Cardiol. 1987 May-Jun;82(3):279-89 - PubMed
  2. Circulation. 1988 May;77(5):1125-38 - PubMed
  3. Circulation. 1986 Apr;73(4):837-46 - PubMed
  4. Circ Res. 1990 Jun;66(6):1461-73 - PubMed
  5. Circ Res. 1976 Nov;39(5):678-83 - PubMed
  6. J Cardiovasc Pharmacol. 1988;12 Suppl 1:S8-14 - PubMed
  7. Eur J Pharmacol. 1989 Feb 7;160(3):349-58 - PubMed
  8. Eur J Pharmacol. 1986 Aug 15;127(3):261-5 - PubMed
  9. J Mol Cell Cardiol. 1986 Mar;18(3):255-63 - PubMed
  10. Circulation. 1980 Apr;61(4):768-78 - PubMed
  11. J Mol Cell Cardiol. 1984 Nov;16(11):1023-36 - PubMed
  12. Circ Res. 1990 Feb;66(2):478-85 - PubMed
  13. J Mol Cell Cardiol. 1980 Jun;12(6):579-93 - PubMed
  14. Nature. 1983 Sep 8-14;305(5930):147-8 - PubMed
  15. Cardiovasc Res. 1985 Jun;19(6):363-9 - PubMed
  16. Cardiovasc Res. 1987 Dec;21(12 ):886-91 - PubMed
  17. Pflugers Arch. 1977 Oct 19;371(1-2):71-6 - PubMed
  18. Circ Res. 1981 Aug;49(2):364-81 - PubMed
  19. J Mol Cell Cardiol. 1986 Apr;18(4):389-99 - PubMed
  20. Circulation. 1986 Nov;74(5):1137-46 - PubMed
  21. Science. 1954 Feb 12;119(3085):200-3 - PubMed
  22. J Physiol. 1985 Jun;363:463-80 - PubMed
  23. Am J Physiol. 1977 Jan;232(1):H85-94 - PubMed
  24. Basic Res Cardiol. 1990 Jan-Feb;85(1):33-44 - PubMed
  25. Naunyn Schmiedebergs Arch Pharmacol. 1989 Nov;340(5):567-75 - PubMed
  26. Circ Res. 1983 Feb;52(2 Pt 2):I129-38 - PubMed
  27. Circ Res. 1983 Apr;52(4):442-50 - PubMed
  28. Br J Pharmacol. 1986 Sep;89(1):137-47 - PubMed
  29. J Cardiovasc Pharmacol. 1989 Aug;14(2):331-40 - PubMed
  30. J Mol Cell Cardiol. 1990 Nov;22(11):1259-72 - PubMed
  31. Am J Physiol. 1975 Sep;229(3):570-81 - PubMed
  32. J Mol Cell Cardiol. 1987 Oct;19 Suppl 5:35-44 - PubMed

Substances

MeSH terms

Publication Types

LinkOut - more resources