Effect of Calcium Channel Blockers on the Na+/K+-ATPase α Isoform Expression in Cultured Aortic Smooth Muscle Cells
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Na+, K+-ATPase is a membrane-bound enzyme which is responsible for maintaining the homeostasis of a cell's Na+-K+ gradient. It has been shown that this enzyme plays a role in the pathogenesis of hypertension (SonguMize et al., 1993). The hypothesis being that blood pressure may be regulating the isoforms of Na+, K+-ATPase. To confirm this hypothesis, aortic smooth muscle cells (ASMC) were exposed to mechanical stretch with the purpose focusing on the expression of the isoforms. The results showed that there was an up regulation in the isoform regulation (Songu-Mize et al., 1996). Currently, there are no studies which have isolated the reason why stretch causes changes in the isoform regulation. It is known that stretch activates Na+, K+ and Ca2+ channels and it may be due to one or a combination of these ions which causes the changes. Because there are no selective stretch-activated channel blockers, the affects of these ions on non-stretched cells must be examined. This experiment deals with the effects of the Ca2+ ion on non-stretched ASMC. A Ca2+ channel blocker (isradipine) was added to a culture of ASMC in an attempt to show its effects on the isoforms of Na+, K+ATPase. It was shown by this experiment that isradipine causes a downregulation of the α1 isoform. Due to technical difficulties, we cannot make any definitive statements about the α2 isoform. With this information, we can now speculate on a possible mechanism by which stretch affects isoform expression.