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OtherCARDIOVASCULAR PHARMACOLOGY

Calcium-Activated Potassium Channels and Nitrate-Induced Vasodilation in Human Coronary Arteries

Rostislav Bychkov, Maik Gollasch, Tobias Steinke, Christian Ried, Friedrich C. Luft and Hermann Haller
Journal of Pharmacology and Experimental Therapeutics April 1998, 285 (1) 293-298;
Rostislav Bychkov
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Maik Gollasch
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Tobias Steinke
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Christian Ried
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Friedrich C. Luft
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Hermann Haller
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Abstract

In some but not all arterial beds, smooth muscle cell calcium-activated K+ channels (KCa channels) play a central role in the mediation of the vasodilator response to nitric oxide (NO) and other nitrates. We investigated the effect of nitrates on KCa channels in the relaxation of human coronary arteries by means of isometric contraction experiments in arterial rings. We also measured whole-cell currents in freshly isolated human coronary artery vascular smooth muscle cells via the patch-clamp technique. Sodium nitroprusside, diethylamine-nitric oxide complex sodium salt and isosorbide mononitratre completely relaxed rings preconstricted with 5 μM serotonin and produced dose-dependent relaxations of 5 μM serotonin-preconstricted human rings. The relaxations were inhibited by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-oxyl 3-oxide (10 μM), which neutralizes nitric oxide. The KCa channel blockers iberiotoxin (100 nM) and tetraethylammonium ions (1 mM) significantly inhibited SNP-induced relaxations of human coronary arteries. Moreover, in the patch-clamp experiments, SNP (1 μM) stimulated KCa currents and spontaneous transient outward K+ currents carried by Ca spark activated KCachannels. The SNP-induced (1 μM) KCa current was strongly inhibited by iberiotoxin (100 nM). These data show that activation of KCa channels in smooth muscle cells contributes to the vasodilating actions of nitrates and nitric oxide in human coronary arteries. This finding may have unique clinical significance for the development of antianginal and antihypertensive drugs that selectively target K+ channels and Ca sparks..

Footnotes

  • Send reprint requests to: Hermann Haller, M.D., Franz Volhard Clinic, Virchow-Klinikum, Wiltbergstraβe 50, 13125 Berlin, Germany.

  • ↵1 This work was supported by the Deutsche Forschungsgemeinschaft, by the Bundesministerium für Forschung und Technologie, and by the Alexander von Humboldt Foundation.

  • ↵2 Present address: Department of Pharmacology, University of Vermont Medical Research Facility, 55A South Park Drive, Colchester, VT 05446.

  • Abbreviations:
    EGTA
    ethyleneglycol bis(oxyethylenenitrilo)tetra-acetic acid
    DMSO
    dimethylsulfoxide
    KCa channel
    calcium-activated K+ current
    Kdr
    delayed rectifier K+ channel
    KATP channel
    ATP-dependent K+ channel
    PTIO
    2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-oxyl 3-oxide
    DEA-NO
    diethylamine-nitric oxide complex sodium salt
    SNP
    sodium nitroprusside
    STOC
    spontaneous transient outward K+current
    IMN
    isosorbide mononitratre
    NO
    nitric oxide
    • Received March 11, 1997.
    • Accepted December 23, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 285, Issue 1
1 Apr 1998
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OtherCARDIOVASCULAR PHARMACOLOGY

Calcium-Activated Potassium Channels and Nitrate-Induced Vasodilation in Human Coronary Arteries

Rostislav Bychkov, Maik Gollasch, Tobias Steinke, Christian Ried, Friedrich C. Luft and Hermann Haller
Journal of Pharmacology and Experimental Therapeutics April 1, 1998, 285 (1) 293-298;

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OtherCARDIOVASCULAR PHARMACOLOGY

Calcium-Activated Potassium Channels and Nitrate-Induced Vasodilation in Human Coronary Arteries

Rostislav Bychkov, Maik Gollasch, Tobias Steinke, Christian Ried, Friedrich C. Luft and Hermann Haller
Journal of Pharmacology and Experimental Therapeutics April 1, 1998, 285 (1) 293-298;
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