Abstract
The mechanism of the long-term inhibitory effect of a dihydropyridine Ca 2+ channel blocker, nisoldipine, on contraction and cytosolic Ca 2+ level ([Ca 2+] i) was examined in isolated rat aorta. Nisoldipine inhibited the [Ca 2+] i and muscle tension induced by high K +. The inhibitory effects were antagonized by a Ca 2+ channel activator, 100 nM Bay k8644, and by a high concentration of Ca 2+ (6.5 mM). Ultraviolet light, which has been shown to decompose dihydropyridines, attenuated the effects of nisoldipine. After nisoldipine had been removed from muscle bath, the inhibitory effect faded away slowly. The residual inhibitory effects on [Ca 2+] i and muscle tension were antagonized by Bay k8644, high Ca 2+ and ultraviolet light. These results suggest that the inhibitory effect of nisoldipine is caused by a decrease in [Ca 2+] i as a result of inhibition of L-type Ca 2+ channels, and that the residual inhibitory effects are caused by the same mechanism as the inhibitory effects of nisoldipine, namely the tight binding of nisoldipine to Ca 2+ channels even after washout.
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