Hayashi-Morimoto R, Yoshitomi T, Ishikawa H, Hayashi E, Sato Y
Department of Ophthalmology, Kitasato University School of Medicine, Kitasato University, Kanagawa, Japan.
Graefes Arch Clin Exp Ophthalmol. 1999 Aug;237(8):661-7. doi: 10.1007/s004170050294.
We set out to clarify the mechanisms involved in the effectiveness of beta-adrenergic receptor antagonists on the ocular circulation.
The effects of three beta antagonists, timolol, betaxolol and carteolol, on the isolated rabbit ciliary artery were investigated in vitro using isometric tension recording methods.
Phenylephrine dose-dependently contracted ciliary artery smooth muscle, and bunazosin (1 microM) shifted this dose-response curve to the right. Isoproterenol, on the other hand, had no effect up to the concentration of 1 mM. Betaxolol and timolol had no effect on the ciliary artery. However, carteolol dose-dependently contracted this muscle from a concentration of 1 microM. After precontraction by excess-[K]0 solutions, application of betaxolol or timolol dose-dependently provoked relaxation; the minimum concentration of betaxolol or timolol required to generate the relaxation was 100 microM and 300 microM, respectively. Carteolol did not generate relaxation at concentrations up to 1 mM. After pretreatment with L-NAME (300 microM), the amplitude of relaxation induced by 10 microM carbachol was reduced to 33.0+/-20.2%, while betaxolol- or timolol-induced relaxation was unchanged. Diltiazem (10 microM) induced relaxation which was not inhibited by pretreatment with L-NAME.
Betaxolol and timolol could directly relax rabbit ciliary artery in vitro at relatively high concentrations, and relaxation was not due to NO released from the preparation. Presumably, this relaxation occurs through action similar to Ca antagonists. However, the clinical importance of this effect is not yet clear. Carteolol had no relaxant effect in vitro.
我们旨在阐明β-肾上腺素能受体拮抗剂对眼循环有效性的相关机制。
采用等长张力记录法，在体外研究了三种β受体拮抗剂（噻吗洛尔、倍他洛尔和卡替洛尔）对离体兔睫状动脉的作用。
去氧肾上腺素剂量依赖性地收缩睫状动脉平滑肌，布那唑嗪（1微摩尔）使该剂量反应曲线右移。另一方面，异丙肾上腺素在浓度高达1毫摩尔时无作用。倍他洛尔和噻吗洛尔对睫状动脉无作用。然而，卡替洛尔从1微摩尔浓度开始剂量依赖性地收缩该肌肉。在用过量[K]0溶液预收缩后，应用倍他洛尔或噻吗洛尔剂量依赖性地引起舒张；产生舒张所需的倍他洛尔或噻吗洛尔的最低浓度分别为100微摩尔和300微摩尔。卡替洛尔在浓度高达1毫摩尔时未产生舒张。用L-精氨酸甲酯（300微摩尔）预处理后，10微摩尔卡巴胆碱诱导的舒张幅度降至33.0±20.2%，而倍他洛尔或噻吗洛尔诱导的舒张未改变。地尔硫䓬（10微摩尔）诱导的舒张不受L-精氨酸甲酯预处理的抑制。
倍他洛尔和噻吗洛尔在相对高浓度时可在体外直接舒张兔睫状动脉，且舒张并非由于标本释放一氧化氮。推测这种舒张通过类似于钙拮抗剂的作用发生。然而，这种效应的临床重要性尚不清楚。卡替洛尔在体外无舒张作用。
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