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- W3150426327 abstract "A recent study indicated that apamin-sensitive current (IKAS, mediated by apamin-sensitive small con- ductance calcium-activated potassium channels subunits) density significantly increased in heart failure and led to recurrent spontaneous ventricular fibrillation. While the underlying molecular correlation with SK channels is still undetermined, we hypothesized that they are remodeled in HF and that bisoprolol could reverse the remodeling. Volume-overload models were created on male Sprague- Dawley rats by producing an abdominal arteriovenous fistula. Confocal microscopy, quantitative real-time PCR, and western blot were performed to investigate the expression of SK channels and observe the influence of b- blocker bisoprolol on the expression of SK channels IKAS, and the effect of bisoprolol on IKAS and the sensitivity of IKAS to (Ca 2? )i at single isolated cells were also explored using whole-cell patch clamp techniques. SK channels were remodeled in HF rats, displaying the significant increase of SK1 and SK3 channel expression. After the treatment of HF rats with bisoprolol, the expression of SK1 and SK3 channels was significantly downregulated, and bisoprolol effectively downregulated IKAS density as well as the sensitivity of IKAS to (Ca 2? )i. Our data indicated that the expression of SK1 and SK3 increased in HF. Bisoprolol effectively attenuated the change and downregulated IKAS density as well as the sensitivity of IKAS to (Ca 2? )i." @default.
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- W3150426327 date "2013-01-01" @default.
- W3150426327 modified "2023-09-27" @default.
- W3150426327 title "Bisoprolol reversed small conductance calcium-activated potassium channel (SK) remodeling in a volume-overload rat" @default.
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