蕪城 俊克

Transforming growth factor beta (TGF-beta) transduces signals through mediation of type I and type II serine/threonine kinase receptors. The expression of TGF-beta type I (T beta R-I) and II (T beta R-II) receptors in rat eyes was investigated immunohistochemically. T beta R-I and T beta R-II immunoreactivity was detected in corneal and conjunctival epithelial cells, corneal endothelial cells, ciliary epithelial cells, lens epithelial cells, retinal pigment epithelial cells, and choroidal vessels. This co-expression of T beta R-I and T beta R-II indicates that the above cells respond to TGF-beta and, because TGF-beta is reported to be produced in ocular tissues, that it may have important autocrine and/or paracrine roles in the growth and metabolism of ocular tissues in situ.

We investigated the effects of long-term instillation of bunazosin hydrochloride--alpha 1 specific adrenergic antagonist--on the aqueous humor dynamics and blood-aqueous barrier in rabbit eyes. We examined intraocular pressure, aqueous flow rate, and blood-aqueous barrier permiability for albumin after four weeks application of 0.05% bunazosin. The effect of bunazosin on blood-aqueous barrier destruction by laser iridophotocoagulation was also examined. During four weeks, bunazosin reduced the intraocular pressure by 1.7 +/- 0.6 mmHg (mean +/- SEM). Continuous application of bunazosin had no significant influence on aqueous flow rate and fluorescein isothiocyanate-labeled rabbit albumin (FITC-Alb) concentration in the anterior chamber. Bunazosin had no effect on the rise of the FITC-Alb concentration after iris photocoagulation, but the intraocular pressure in bunazosin treated eyes was significantly lower than in control eyes one hour after photocoagulation.