Magnesium induced vascular relaxation and role of Calcium-dependent K+ Channels

Abstract

Background and objectives: Magnesium is established as a neuro-protective agent and now also known as a vasodilator. It 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 cells from rabbit basilar artery.

Material and Methods: Fresh smooth muscle cells were isolated from the basilar artery by enzyme treatment. Whole cell current recording was done using patch-clamp technique. Appropriate bath solution was used to have potassium current. The effect of Magnesium was observed and to identify the potassium (K⁺) channel involved in the magnesium-induced currents, different potassium channel blockers were used.

Results: Magnesium increased the step pulse-induced outward K⁺ currents by more than fortyfive percent over control level (p<0.01). The outward K⁺ current was decreased significantly by application of tetraethylammonium, a non-specific K⁺ channel blocker, and by iberiotoxin, a largeconductance Ca²⁺-activated K⁺ (BK_Ca) channel blocker, but was not inhibited by glibenclamide an ATP-sensitive K⁺ (K_ATP) channel blocker. Magnesium failed to increase the outward K+ currents in the presence of IBX.

Conclusion: These results demonstrate that calcium dependent pottassium (BK_Ca) channels has role in magnesium induced vascular relaxation in rabbit basilar smooth muscle cells and needs to be worked out for human.

DOI: http://dx.doi.org/10.3126/jmcjms.v1i1.7880

Janaki Medical College Journal of Medical Sciences (2013) Vol. 1 (1):9-13