Vascular effect of various antiglaucoma agent on ciliary artery smooth muscle cells.

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Though it is generally accepted that decreasing intraocular pressure (IOP) is important to treat normal tension glaucoma (NTG), increasing ocular vascular perfusion is also considered to be important. The purpose of this study is to clarify the vasodilatory mechanism of various compound used for treatment of glaucoma, pharmacologically. We have investigated the effect of beta antagonists or prostaglandin related compounds on isolated rabbit and rat ciliary artery in vitro. These compound were reported to have effect on ocular circulation in addition to decrease IOP. Betaxolol dose-dependently relax rabbit ciliaryn artery by action similar to Ca antagonists. NIpradilol, another be-ta antagonist used for treatment of glaucoma, also relax rabbit ciliary artery as NO-donor. Levobumolol also relax this muscle by changing intracellular calcium sensitivity. All these be-ta antagonists relax rabbit ciliary artery by different mechanisms all which are not be-ta receptor antagonistic action. Unoprostone, a prostaglandin related compound also used for treatment of glaucoma, relax this muscle. The mechanism of muscle relaxation by unoprostone may be mediated by inhibition of Ca^<2+> entry, possibly through capacitative Ca^<2+> channels. Latanoprost, another prostaglandin related compound and stronger capability of reducing IOP also relax rabbit ciliary artery but the action is weaker than unoprostone. These results indicate that many antiglacoma agents relax vascular smooth muscle by various mechanisms which is different from the mechanisms of reducing IOP. These findings may provide useful information for developing new drugs for improving ocular circula