Types of pharmacological action at autonomic ganglia / by W.D.M. Paton.

  • William Paton
Date:
1954
Catalogue details

Licence: In copyright

Credit: Types of pharmacological action at autonomic ganglia / by W.D.M. Paton. Source: Wellcome Collection.

    15/20 (page 279)
    D. — Non-basic substances. This category includes a number of miscellaneous compounds. First may be mentioned the barbiturates (Exley, 1952) some of which may be quite active in interfering with ganglionic transmission; it is not quite established how this occurs but it is probably by depression of acetylcholine release. Second are the important group of general anaesthetics (Larrabee and Posternak, 1952). Although a number of these are known to interfere with ganglionic transmission, too little is known about the mechanism still. Another group consist of the digitalis glycosides, which Konzett and Rothlin (1952), found to potentiate the effect of acetylcholine on the ganglion. Conclusion We can now recognize four main groups of gangiionically active substances (and hence four main groups of pharmacological actions) : — a) Quaternary compounds, or compounds closely related to acetyl¬ choline, which imitate, compete with, preserve, or sensitize to the natural transmitter. The actions of all these drugs are interpretable in terms of the classical experiments on ganglionic transmission, and are tested usually by repeating certain of these classical experiments. b) Amines which depress ganglionic transmission and antagonize the effects of injected ganglion stimulants, but are also able to interfere with acetylcholine release and to depress nervous conduction. These are a variegated group, not yet properly defined. c) Inorganic ions capable of stimulating or depressing nerve endings or ganglion cell. d) A miscellaneous group including substances such as digitalis, barbiturates, or general anaesthetics. At least eight types of action must thus be disentangled : 1) Specific ganglion depolarization; 2) Specific ganglion block (competitive); 3) Anticholinesterase action; 4) Sensitization to depolariza¬ tion; 5) Depression of transmitter release; 6) xAntagonism to ganglion depolarization (non-specific); 7) Stimulation of transmitter release; 8) Stimulation of ganglion cells (non-specific direct action). It seems clear that although one thinks at first that the actions of most drugs at the ganglionic level are fairly well understood, it is in fact only a handful of them that have been adequately studied. Our main need,