Role of endothelium‐derived nitric oxide in the regulation of tonus in large‐bore arterial resistance vessels, arterioles and veins in cat skeletal muscle

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Abstract
The role of endothelium‐derived nitric oxide in the regulation of vascular resistance (tonus) in cat skeletal muscle was studied with the use of NG‐monomethyl‐l‐arginine (L‐NMMA), a specific inhibitor of nitric oxide formation from l‐arginine. The study was performed with a whole‐organ technique which permits simultaneous, continuous and quantitative recordings of resistance reactions in the whole vascular bed (Rt /Sb>) and in its three consecutive sections: large‐bore arterial resistance vessels (>25 μm; Ra. prox) small arterioles (< 25 μm; Ra, miero) and veins (Rv. NG‐monomethyl‐L‐arginine (3–100 mg kg‐1 tissue, i.a.) induced a dose‐dependent increase in resistance that was preferentially, but not selectively, confined to the large‐bore arterial resistance vessels. At a maximally effective dose (100 mg kg‐l), the nitric oxide inhibitor caused a marked constriction, within 5 min, on average increasing Rt by 99%, Ra, prox by 138%, Ra, miero by 18% and Rv by 23%. The constrictor response to Ng‐monomethyl‐L‐arginine was long‐lasting but disappeared gradually over a period of about 1 h. However, it could be abruptly abolished by excess L‐arginine (300 mg kg‐1, i.a.). The vasodilator response (Rt) to acetylcholine was significantly attenuated in the presence of N'‐monomethyl‐L‐arginine compared with the control response. The results suggested that nitric oxide formation from L‐arginine by the vascular endothelium plays a fundamental role in the regulation of vascular resistance (tone) in vivo, with its main site of action located in the large‐bore arterial resistance vessels.

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