Current eye research · 2001
The effect of angiotensin II on uveoscleral outflow in rabbits.
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Inoue T, Yokoyoma T, Koike H
Аннотация
PURPOSE: In our previous study, we showed that the AT1 receptor antagonist increased uveoscleral outflow (USF) when topically applied to the rabbit eye. However this increase was too small to demonstrate a clear physiological role for ocular angiotensin II (AII). Hence, the purpose of this study was to determine whether ocular AII influenced USF regulation, and if so, how this occurred.
METHODS: USF was measured by the FITC-dextran perfusion method in albino rabbits. AII and its receptor antagonists were directly applied into the anterior chamber by adding into the perfusate and by perfusing with FITC-dextran. We also analyzed angiotensin receptors on the rabbit ciliary body membrane by a receptor binding assay with 125I-[Sar1), Ile8]-AII as a ligand.
RESULTS: CS-088 (1 microg/ml) increased USF by 24% while AII decreased USF in a concentration-dependent manner between 10 and 500 nM. Its maximum decrease of 19% occurred at 500 nM. At this AII concentration the USF reduction was antagonized by 1 microg/ml CS-088, an AT1-receptor antagonist, but not by the same concentration of PD-123,177, an AT2-receptor antagonist. Specific 125I-[Sar1, Ile8]-AII binding to the rabbit ciliary body membranes was inhibited by CS-088 with an inhibition constant of 7.05 nM, whereas inhibition by PD-123,177 was not observed.
CONCLUSIONS: Ocular AII was indicated to attenuate USF via AT1 receptors in rabbits, however its physiological effect was not critical in IOP regulation.
METHODS: USF was measured by the FITC-dextran perfusion method in albino rabbits. AII and its receptor antagonists were directly applied into the anterior chamber by adding into the perfusate and by perfusing with FITC-dextran. We also analyzed angiotensin receptors on the rabbit ciliary body membrane by a receptor binding assay with 125I-[Sar1), Ile8]-AII as a ligand.
RESULTS: CS-088 (1 microg/ml) increased USF by 24% while AII decreased USF in a concentration-dependent manner between 10 and 500 nM. Its maximum decrease of 19% occurred at 500 nM. At this AII concentration the USF reduction was antagonized by 1 microg/ml CS-088, an AT1-receptor antagonist, but not by the same concentration of PD-123,177, an AT2-receptor antagonist. Specific 125I-[Sar1, Ile8]-AII binding to the rabbit ciliary body membranes was inhibited by CS-088 with an inhibition constant of 7.05 nM, whereas inhibition by PD-123,177 was not observed.
CONCLUSIONS: Ocular AII was indicated to attenuate USF via AT1 receptors in rabbits, however its physiological effect was not critical in IOP regulation.