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Endothelium‐derived relaxing factor released by 5‐HT: distinct from nitric oxide in basilar arteries of normotensive and hypertensive rats

1 The role of the endothelium in cerebrovascular responses to 5‐hydroxytryptamine (5‐HT) was investigated in spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto rats (WKY) in vitro. 2 Cumulative addition of 5‐HT caused concentration‐dependent contractions in ring preparations of SHR basilar arteries; the contractile response was smaller in WKY basilar arteries. 3 Removal of the endothelium enhanced markedly the contractile responses to 5‐HT in WKY arteries but had only a slight effect in SHR arteries. The responsiveness to 5‐HT in WKY arteries after removal of endothelium was comparable to that in SHR arteries. 4 The endothelium‐dependent relaxation induced by acetylcholine in WKY basilar arteries was almost abolished by treatment with 10 μm methylene blue or 10 μm NG‐nitro‐l‐arginine (l‐NOARG). However, the response to 5‐HT was not affected by treatment with methylene blue, l‐NOARG or indomethacin. 5 Application of 10–20 mm K+ or 3.2 mm tetraethylammonium (TEA) did not change significantly, or only increased slightly, the resting tension, but markedly enhanced the contractile response to 5‐HT in WKY arteries with endothelium. In contrast, the submaximal response to 5‐HT in SHR arteries with endothelium was significantly enhanced by 0.3 mm TEA. 6 In the presence of 1 mm TEA, the application of 10 μm l‐NOARG further enhanced the responses of 5‐HT in WKY arteries with endothelium. In SHR arteries with endothelium, 10 μm l‐NOARG per se enhanced slightly but significantly the responses to 5‐HT. 7 These results indicate that 5‐HT‐induced contraction in basilar arteries is substantially attenuated by an endothelium‐dependent mechanism in WKY, but to a much lesser extent in SHR. The major relaxing factor released by 5‐HT from endothelium in WKY is distinct from NO and may exert its effect by activating K+ channels.