Martin X
Clinique Ophtalmologique Universitaire de Zurich, Suisse.
Ophtalmologie. 1990 Mar-Apr;4(2):154-5.
If beta-blockage does not cause lowering of aqueous humor secretion, in itself responsible for the maintenance of intraocular pressure, what is the mechanism of action? The antagonism for indolamines, recently measured in aqueous humor, the absence of nocturnal effect, and the amplitude diminution of diurnal variations thus produced suggest that beta-blockers could interact with indolamines, since the latter are probably responsible for intraocular pressure regulation. Aqueous humor secretion depends to a major extent on the sodium-potassium pump and its enzyme, Na+K(+)-ATPase. Serotonin, known for its activating action on Na+K(+)-ATPase, is present in the greatest amounts in the morning, precisely when the aqueous humor secretion is the highest. Moreover, timolol is a potent antagonist of serotonin, suggesting that beta-blockers could decrease the secretion by antagonism with serotonin at the level of Na+K(+)-ATPase. Since serotonin is metabolized to melatonin during sleep, beta-blockers might simulate a state of sleep of the ciliary epithelium.
如果β受体阻滞剂本身不会导致房水分泌减少（而房水分泌减少才是维持眼压的关键因素），那么其作用机制是什么呢？近期在房水中检测到的对吲哚胺的拮抗作用、无夜间效应以及由此产生的昼夜变化幅度减小表明，β受体阻滞剂可能与吲哚胺相互作用，因为后者可能负责眼压调节。房水分泌在很大程度上依赖于钠钾泵及其酶——Na+K(+)-ATP酶。血清素对Na+K(+)-ATP酶具有激活作用，其在早晨的含量最高，而此时房水分泌恰好也处于最高水平。此外，噻吗洛尔是血清素的强效拮抗剂，这表明β受体阻滞剂可能通过在Na+K(+)-ATP酶水平上拮抗血清素从而减少房水分泌。由于血清素在睡眠过程中会代谢为褪黑素，β受体阻滞剂可能会模拟睫状上皮的睡眠状态。
