1. Archive
2. Vol.52, No.3

Development of Pressurized Retinal Resistance-Sized Arteriolar Preparation with Special Reference to Acetylcholine-Induced Nitric-Oxide–Mediated Vasodilatation

Abstract: We examined the responses of pressurized bovine retinal functional arterioles (97–185 μm in diameter and ∼3 mm long) to vasoactive substances and the mode of action of acetylcholine (ACh) on the pressurized arterioles. The retinal arterioles were cannulated at both ends with glass micropipettes and perfused at a constant pressure of 60 mmHg. Vasoconstrictions of the retinal arterioles were induced by prostaglandin F_2α (PG F_2α), U46,619, noradrenaline (NA), and 5-hydroxytryptamine (5-HT) in a dose-dependent manner. The decreasing order of potency (pD₂ value) in the constrictive responses was as follows: 5-HT = U46,619 > NA > PG F_2α. On the other hand, sodium nitroprusside (SNP), isocarbacyclin (a stable prostaglandin I₂ analog), ACh, and isoproterenol (ISP) caused dose-dependent vasodilatation in the pressurized retinal arterioles preconstricted with high-potassium solution (40 mM K⁺). The decreasing order of potency in the vasodilative responses was as follows: isocarbacyclin > SNP > ACh. The ACh-induced vasodilatation was suppressed significantly by pretreatment with Nω-nitro-L-arginine methyl ester (L-NAME) (3 × 10⁻⁵ M). A treatment with L-arginine (10⁻³ M) in the presence of 3 × 10⁻⁵ M L-NAME reversed completely the L-NAME–induced reduction of the vasodilatation. These results suggest that ACh causes the production and release of endogenous nitric oxide or its related compounds, which results in vasodilatation of the pressurized bovine retinal functional arterioles.

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