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To elucidate the effects of various chemical mediators, which are considered to appear in inflammation, on vascular smooth muscle, annular specimens of porcine lingual arterial smooth muscle were prepared, and divided into specimens denuded or undenuded of vascular endothelium. These specimens were attached to the thermostat incubator of an intracellular calcium ion concentration measurement unit, stimulated with 40 mM KCl, noradrenalin (NA), or U46619, followed by administration of acetylcholine (ACh) or bradykinin (BK), and the isometric contractile tension generated and fluorescence intensity ratio were simultaneously measured ; the following conclusions were drawn. 1. The inhibition by ACh or BK of NA-, high KCl-, or U46619-induced contraction was dependent on the presence of vascular endothelium, suggesting the involvement of a decreased [Ca^<2+>]_i concentration in the contraction inhibition. 2. It was suggested that the inhibition of high KCl-induced contraction by ACh or BK was weaker than that of receptor stimulation-induced contraction. 3. The administration of BK showed biphasic changes in U46619-induced contractile tension and [Ca^<2+>]_i.
