Atorvastatin exerts non-lipid-lowering vasculoprotective effects by reversing IL-1β-induced depolarization in smooth muscle cells via BK channel activation.
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May indicate non-lipid vasculoprotective effects via BK channels; hypothesis-generating in animals, no practice change.
Statins are known to exert vasculopretective effects which are independent of their cholesterol lowering ability. The aims of this study were to investigate a possible effect of atorvastatin on Ca2+-activated K+ channels (BK) in cultured rat aorta smooth muscle cells (ASMCs) and to assess their contribution to interleukin-1β (IL-1β) induced changes of membrane potential and BK activity. The membrane potential was determined by the intensity of DiBAC4 (3) detected under confocal microscope. We found that atorvastatin hyperpolarized ASMCs in a concentration-dependent manner. 100 μmol atorvastatin activated BK channel directly which is determined by patch-clamp experiments. 12 h treatment of IL-1β resulted in decreased BK channel activity and depolarization of the cells, while atorvastatin or hydrogen dioxide (H2O2) scavenger catalase completely abolished the effects. There was no synergistic effect when catalase and atorvastatin were applied together. Furthermore, perfusion with atorvastatin resulted in a similar pattern of BK activation with hyperpolarization of ASMCs treated with IL-1β, which have significant differences statistically in comparison with saline group. Our results provide a potential important molecular mechanism of non-lipid-lowering effects of the atorvastatin by modulating BK channel.
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Ying Yang (2011) studied this question.
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