L-type voltage-dependent Ca2+ and ATP-sensitive K+ channels are not involved in the regulation of bovine ciliary muscle contractility.

We 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 microM), 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 microM) diltiazem (10 microM) and verapamil (1 microM), 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 microM, did not contract ciliary muscle partially depolarized with 10 mM KCl, whereas at 0.01 and 0.1 microM it contracted partially depolarized rabbit aortae. Furthermore, diazoxide (100 microM), 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 microM), 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 contractility.