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Hydralazine-induced vasodilation involves opening of high conductance Ca2+-activated K+ channels

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The purpose of this study was to investigate whether high conductance Ca2+-activated K+ channels (BK(Ca)) are mediating the vasodilator action of hydralazine. In isolated porcine coronary arteries, hydralazine (1-300 microM), like the K+ channel opener levcromakalim, preferentially relaxed contractions induced by K+ (20 mM) compared with K+ (80 mM). In addition, concentration-relaxation curves for hydralazine (pD2 = 5.38 +/- 0.06; Emax = 85.9 +/- 3.6%) were shifted 10-fold to the right by the BK(Ca) blockers tetraethylammonium (1 mM) and iberiotoxin (0.1 microM). In contrast, nimodipine (a Ca2+-entry blocker), relaxed contractions induced by K+ (20 mM) and K+ (80 mM) equally and nimodipine-induced relaxations were neither antagonized by tetraethylammonium nor by iberiotoxin. In isolated perfused rat hearts, hydralazine (1 microM) increased coronary flow by 28.8 +/- 2.7%. Iberiotoxin (0.1 microM) suppressed this response by 82% (P < 0.05). In conscious, chronically catheterized rats the hypotensive response to hydralazine (0.6 mg kg(-1) min(-1)) was significantly reduced by 41% during infusion of iberiotoxin (0.1 mg kg(-1)). It is concluded, that opening of BK(Ca) takes part in the mechanism whereby hydralazine produces vasodilation.

Original languageEnglish
JournalEuropean Journal of Pharmacology
Volume361
Issue number1
Pages (from-to)43-9
Number of pages7
ISSN0014-2999
Publication statusPublished - 13 Nov 1998

    Research areas

  • Animals, Blood Pressure, Calcium, Carcinogens, Cattle, Consciousness, Coronary Vessels, Cromakalim, Dose-Response Relationship, Drug, Electrophysiology, Heart, Hydrazines, In Vitro Techniques, Male, Nimodipine, Patch-Clamp Techniques, Peptides, Potassium, Potassium Channels, Rats, Swine, Tetraethylammonium, Vasodilation, Vasodilator Agents

ID: 44934019