Abstract
The purpose of this study was to investigate whether high conductance Ca 2+-activated K + channels (BK Ca) are mediating the vasodilator action of hydralazine. In isolated porcine coronary arteries, hydralazine (1–300 μM), 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 (pD 2=5.38±0.06; E max=85.9±3.6%) were shifted 10-fold to the right by the BK Ca blockers tetraethylammonium (1 mM) and iberiotoxin (0.1 μM). In contrast, nimodipine (a Ca 2+-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 μM) increased coronary flow by 28.8±2.7%. Iberiotoxin (0.1 μM) 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.
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