Systemic and ocular vascular roles of the antiglaucoma agents beta-adrenergic antagonists and Ca2+ entry blockers

This review addresses whether the antiglaucoma agents beta-adrenergic antag onists and Ca2+ entry blockers cause vasoactive effects in the retinal and other ocular vasculatures, as they do in other tissues. The potent vasodila ting effects of Ca2+ entry blockers oil ocular vessels have recently been d emonstrated in in vivo and in vitro studies, implying that the maintenance of ocular vascular tone relies almost exclusively on extracellular Ca2+. Ca 2+ entry blockers may potentially play a role in relaxing the retinal, long posterior ciliary, and ophthalmociliary arteries to improve the ocular cir culation in vascular diseases in which there is considerable vascular tone present. The beta-adrenergic antagonists are discussed with reference to th eir antihypertensive role, their effect on other vascular beds, and finally what is known of their effect in the ocular vasculature. The emerging evid ence that particular selective beta-adrenergic antagonists, such as betaxol ol, are also potent Ca2+ channel entry blockers in other vascular beds is p resented. Betaxolol has been shown to induce vasodilatation in the retinal and other ocular vascular beds, although studies have shown that beta(1)-ad renergic receptors are sparse in these vascular bells. This implies that an alternative mechanism must be responsible for betaxolol-induced vasodilata tion, Evidence is presented that betaxolol vasodilates via its potent Ca2channel entry blocking properties, and its potency and ability to vasodilat e are compared with those of nimodipine and timolol, as well as with those of other Ca2+ channel entry blockers. Important areas for: future research in this area are discussed. (C) 1999 by Elsevier Science Inc. All rights re served.