On the Influence of Atropine on some Ncotine‐like Actions of Acetylcholine

Summary. Dale'S original definition of the different actions of ac. ch. stated that muscarinelike actions are those which are abolished by atropine, while the nicotinelike actions are not antagonized. Later experiments show that both kinds of actions are antagonized by atropine, even if several exceptions from this rule are described There is, however, a quantitative difference between muscarinelike and nicotinelike actions with regard to the atropine antagonism. As a rule, muscarinelike actions are inhibited by smaller concentrations, while nicotinelike actions require higher concentrations of atropine. This quantitative difference is by some authors looked upon as a criterion of a fundamental distinction between the two kinds of action. The nicotinelike actions require, however, not only larger amounts of atropine, but also large amounts of ac. ch. It seems possible that those properties of an organ which make large amounts of ac. ch. necessary also make it necessary to use large amounts of atropine before the antagonism can be demonstrated. It is shown in the present paper that there is a constant ratio between the amounts of atropine which are necessary to provoke a certain effect on various organs of frog and the amount of atropine which is necessary for diminishing this effect to a certain degree. Thus, the quantitative differences between the two kinds of action with regard to the atropine antagonism do not seem to constitute any real distinction. Striped muscles of frog must be exposed to atropine during 50 to 60 minutes, before the atropine exerts its full antagonistic power. Is has been shown previously that atropine antagonizes the effect of ac. ch. on striped muscles, when these are suspended in a bath, while the effect of intraarterially injected ac. ch. is not abolished. In the latter case too small amounts of atropine seem to have been used. In the present paper is shown that atropine prevents the “quick contractions” of skeletal muscles of frog or rabbit, provoked by intraarterial injections of ac. ch. Those amounts of atropine which abolish the “quick contractions” do not have any influence on the excitability of the muscles through their nerves. If, however, the muscles are suspended in very strong concentrations of atropine they lose at first their indirect excitability and then also their direct excitability. Several reasons—inter alia the effect of d and l‐hyoscyamine—show that this so‐called curare‐action” of atropine is not of the same nature as the ac. ch.‐antagonizing effects of atropine. Thus, while the effects of added ac. ch. is abolished, atropine exerts no action on the indirect excitability which can be explained as an antagonizing of ac. ch. It is emphasized that the theory of humoral transmission at present offers no acceptable explanation of this discrepancy.