Magnesium sulfate suppresses L-type calcium currents on the basilar artery smooth muscle cells in rabbits.

OBJECTIVES

Although magnesium is a well-known treatment for vasospasm following subarachnoid hemorrhage, its mechanism of action for cerebral vascular relaxation is not clear. In addition, it is known that L-type calcium (Ca(2+)) channels play a pivotal role in smooth muscle contraction. To investigate the role of L-type Ca(2+) channels in the magnesium-induced relaxation of basilar smooth muscle cells, we examined the effect of magnesium sulfate on L-type Ca(2+) currents using freshly isolated smooth muscle cells from rabbit basilar arteries.

METHOD: Rabbits were anesthetized with ketamine (50 mg/kg) with xylazine (25 mg/kg) and exsanguinated. Smooth muscle cells were isolated from rabbit basilar arteries by enzyme treatment. Cells were stored at 4°C before use. Whole-cell patch clamp technique was used to identify L-type Ca(2+) currents, using the potassium channel blocker, cesium chloride, and nimodipine and Bay K8644 as a blocker and activator of L-type Ca(2+) channels, respectively.

RESULTS

Inward currents induced by step pulses were significantly reduced by nimodipine (n = 5, P<0·05) and increased by Bay K8644 (n = 5, P<0·05). The L-type Ca(2+) currents (122±14·0 pA, n = 12) were significantly reduced by the application of 5 mM magnesium sulfate (28±4 pA, n = 12, P<0·05). The inward currents enhanced by Bay K8644 were further suppressed by the application of magnesium sulfate.

DISCUSSION: These results demonstrate that L-type Ca(2+) channels are functionally expressed in rabbit basilar smooth muscle cells and suggest that L-type Ca(2+) channels may play a pivotal role for magnesium-induced relaxation.