Abstract
The effect of some cyclic compounds in concns. from about 10-2 to 10-7 mol on the rectus abdominis muscle was investigated. Shortening of the muscle was induced by benzol, phenol, hydroquinone benzaldehyde, acetophenone, [alpha]-napfcthol, [beta]-naphthol, indol and quinoline. Benzol and quinoline were the most effective agents. The acetylcholine sensitivity of muscle was increased by cyclohexanol, benzol,''benzyl alcohol, acetophenone, benzaldehyde, phenol, hydroquinone, [alpha]-naphthol, [beta]-naphthol, m-dinitrobenzene, p-amino phenol, aniline, benzidine, acetanilide, sulfonamides, indol, quinoline, and to a small extent by benzoic acid, salicylic acid, eyclohexane, inositol, naphthalene, diphenylamine, and 1(-)tryptophane. The acetylcholine sensitivity was not modified by toluol, p-amino benzoic acid, potassium phenol sulfonate, acetylsalicylic acid, skatol, indol-3-acetic acid, and carbazole. The acetylcholine sensitivity was decreased by 8-hydroxyquinoline and oleic acid. The K sensitivity was decreased in the presence of acetophenone, benzaldehyde, hydroquinone, benzidine, and the sulfonamides. The K sensitivity was not modified by acetylsalicylic acid, and 1 (-) tryptophane and was increased by the other substances used. The increase of the acetyl-choline sensitivity was caused by both a physostigmine-sensi-tive and another mechanism. Changes of acetylcholine sensitivity often did not parallel the changes of K sensitivity suggesting that acetylcholine and K sensitivity depend, at least partly, on different mechanisms. Shortening of muscle and changes of the sensitivity of muscle to chemical stimuli were probably due not only to the surface activity of the substances but also to as yet unidentified chemical mechanisms.