Abstract
Rat retinae were dissociated to yield intact microvessels 7 to 42 μm in diameter. These were loaded with fura-2 AM and single fragments anchored down in a recording bath. Intracellular Ca2+ levels from 20- to 30-μm sections of vessel were estimated by microfluorimetry. The vessels studied were identified as metarterioles and arterioles. Only the microvascular smooth muscle cells loaded with fura-2 AM and changes in the fluorescence signal were confined to these cells: Endothelial cells did not make any contribution to the fluorescence signal nor did they contribute to the actions of the drugs. Caffeine (10 mM) or elevated K+ (100 mM) produced a transient rise in cell Ca2+ in the larger vessels (diameters >18 μm) but had no effect on smaller vessels (diameters <18 μm). Rises in cell Ca2+ were accompanied by a rapid (∼2 s to peak) contraction followed by relaxation. Caffeine and K+ responses were blocked by ryanodine (10 μM) and nifedipine (1 μM), respectively. In all the vessels tested, vasopressin (arginine, 10 nM) elicited a transient increase in cell Ca2+ and a constriction, irrespective of the diameter of the vessel. All vessels tested also responded to endothelin-1 (1–10 nM) through an EtA receptor to produce a transient rise in cell Ca2+ followed by a plateau phase of elevated Ca2+ and a constriction. In contrast to the transient effects of vasopressin, caffeine, and K+, the cell Ca2+ remained elevated (>30 min) on washing out the endothelin and the vessel failed to relax. These results demonstrate heterogeneity between smaller and larger retinal vessels with regard to Ca2+ mobilisation and homogeneity with respect to the actions of vasoactive peptides.
Published Version
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