ABSTRACTWe compared the effects of L-type voltage-dependent Ca2+and ATP-sensitive K+channels modulators on contractility in isolated bovine ciliary muscle with those in rabbit aortae. Nifedipine (0.1 and 1 μM), a dihydropyridine Ca2+channel blocker, did not relax bovine ciliary muscle precontracted with 100 mM KCl. Nondihydropyridine Ca2+channel blockers, semotiadil fumarate (SD-3211, 1 μM), diltiazem (10 μM) and verapamil (1 μM), did not affect contractility, but at higher concentrations, they all had a relaxant effect. Bay K 8644, a L-type voltage-dependent Ca2+channel activator, even at 1 μM, did not contract ciliary muscle partially depolarized with 10 mM KCl, whereas at 0.01 and 0.1 μM it contracted partially depolarized rabbit aortae. Furthermore, diazoxide (100 μM), an ATP-sensitive K+channel opener, had a relaxant effect on aortae precontracted with 25 mM KCl, but not on ciliary muscle. This relaxation was inhibited by glibenclamide (10 μM), an ATP-sensitive K+channel blocker, indicating that diazoxide relaxes rabbit aortae by activating ATP-sensitive K+channels. These results suggest that L-type voltage-dependent Ca2+and ATP-sensitive K+channels play a minor role in the regulation of bovine ciliary muscle contra
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