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.

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    its sheath). It is, however, at most only a rather weak local anaesthetic. The suggestion that compounds with some degree of local anaesthetic potency should also, by virtue of it, produce the characteristic simultaneous anti-stimulant and anti-release action on ganglia, extends the generalization that such compounds also tend to be quinidine-like, to antagonise acetylcholine on the rectus abdominis, intestine and perfused rabbit’s ear, to cool adrenalectomised rats, to depress histamine bronchoconstriction, and to antagonize adrenaline on the rabbit’s ear. (Dawes, 1946; Burn & Dutta, 1948; Dutta, 1949). It recalls Fleckenstein’s classification of many drugs into “ catelectrotonic ” and “ anelectrotonic ” (Fleckenstein, Wagner and Goggel, 1950); but, despite some analogies between anelectrotonus and local anaesthesia, procaine amide does not hyperpolarize the ganglion; so that such a classification is certainly premature at the ganglion. We can only observe that a large number of amines are able to interfere simultaneously with nervous transmission, with ganglionic trans¬ mission, and with the ganglion response to chemical excitation by nicotinic drugs; that some of them are known to depress acetylcholine release; and to suggest that all these actions may depend on a common membrane stabilisation, to which the fine terminal ramifications of the preganglionic nerves as well as the adjacent neuronal membrane are particularly sensitive. C. — Inorganic ions. The simplest compounds active on autonomic ganglia are ions such as potassium., barium and ammonium. (Brown and Feldberg, 1936; Ambache, 1949; Banister, Hebb and Konzett, 1949). These may act in two ways, either by the excitation of pre-ganglionic terminals so as to cause acetylcholine release (demonstrated for potassium) or by excitation of the ganglion directly. These actions may be distinguished by the fact that the former, but not the latter, is abolished by denervation and by the use of ganglion blocking drugs. Deficiency of calcium (Harvey & Macintosh, 1940) will depress the release of acetylcholine and, at the same time, produce a discharge of the ganglion cell; thus a failure of transmission occurs but post¬ ganglionic activity is still observed. Phosphate compounds, including ATP, exert a stimulant action both on the normal and on the denervated ganglion (Feldberg & Hebb, 1947) and it has been suggested that they work by calcium deprivation. Magnesium causes block, and depresses ACH release (Stanbury, 1948; Huttfjr and Kostial, 1953).