Magnesium increases iberiotoxin-sensitive large conductance calcium activated potassium currents on the basilar artery smooth muscle cells in rabbits.

OBJECTIVES

Magnesium has been known for treating vasospasm following subarachnoid hemorrhage. However, its action mechanism in cerebral vascular relaxation is not clear. Potassium channels play a pivotal role in the relaxation of smooth muscle cells. To investigate their role in magnesium-induced relaxation of basilar smooth muscle cells, we examined the effect of magnesium on potassium channels using the patch clamp technique on acutely isolated smooth muscle cells from rabbit basilar artery.

METHOD

Fresh smooth muscle cells were isolated from the basilar artery by enzyme treatment. To identify which potassium channels are involved in the magnesium-induced currents, we used the potassium channel blockers tetraethylammonium (TEA), glibenclamide, apamin and iberiotoxin (IBX).

RESULTS

Magnesium (5 mM) increased the step pulse-induced outward K+ currents by 46% over control level (P < 0.01). The outward K+ current was decreased to 22% (P < 0.01) by TEA (10 mM), a non-specific K+ channel blocker, and to 60% of control level (P < 0.01) by IBX (0.1 μM,), a large-conductance Ca2+-activated K+ (BK) channel blocker, but was not inhibited by apamin (1 nM), a small-conductance Ca2+ -activated potassium (SK) channel blocker, or glibenclamide (3 mM), an adenosine triphosphate (ATP)-sensitive K+) channel blocker. Caffeine (3 mM) enhanced outward K+ currents. Magnesium-induced increase of outward K+ currents persisted in the presence of apamin. However, magnesium failed to increase the outward K+ currents in the presence of IBX.

DISCUSSION

These results demonstrate that BK channels are functionally expressed in rabbit basilar smooth muscle cells and suggest that BK channels may play a pivotal role in magnesium-induced relaxation.