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PubMed1963

The action of drugs on the circular muscle strip from the guinea-pig isolated ileum.

The circular muscle strip is a new preparation for examining the action of drugs on the circular muscle of the guinea-pig isolated intestine. The preparation differed from the longitudinal muscle in that it was insensitive to drugs which act on autonomic effector tissues but, after inhibition of cholinesterase, it responded readily to choline esters, 5-hydroxytryptamine, histamine and nicotine. This behaviour necessitated the treatment of each strip with the anticholinesterase NN-diisopropylphosphodiamidic fluoride (mipafox) before each experiment. The contractions of the strip by 5-hydroxytryptamine, histamine and nicotine were abolished by procaine, botulinum toxin (Type A), morphine and hemicholinium, whilst the actions of acetylcholine and methacholine were unaffected. Contractions of the strip in response to each of the drugs were abolished by atropine and hyoscine. The action of nicotine was specifically antagonized by hexamethonium, that of 5-hydroxytryptamine by desensitization of the tissue to 5-hydroxytryptamine, and that of histamine either by desensitization of the tissue to histamine or by mepyramine. It is postulated that 5-hydroxytryptamine, histamine and nicotine stimulate specific receptor sites within the intramural nerve plexuses of the guinea-pig isolated ileum. Finally, botulinum toxin (Type A), morphine or hemicholinum, acting on the neuronal elements of the intramural plexuses, depressed the contractions of the circular muscle strip due to histamine or nicotine more readily than those due to 5-hydroxytryptamine.

Acetylcholine↗
PubMed1963

THE ORIGIN OF THE ACETYLCHOLINE RELEASED SPONTANEOUSLY FROM THE GUINEA-PIG ISOLATED ILEUM.

When the guinea-pig isolated ileum had been previously treated with the anticholinesterase, NN-diisopropylphosphodiamidic fluoride (mipafox), and attached to an isotonic lever loaded with 0.5 g, it released acetylcholine into Krebs solution gassed with a mixture of 95% oxygen and 5% carbon dioxide. The amount of acetylcholine spontaneously released depended on the duration of the rest period. Cocaine, procaine or cooling the preparation to 25 degrees C greatly reduced this spontaneous output of acetylcholine, thus providing evidence in support of nervous origin of the ester. Reduction of the calcium ion content of the Krebs solution to one-twentieth of its usual value or increase in the magnesium ion content four-fold, changes which inhibit the release of acetylcholine from somatic motor nerve-endings, inhibited the output of acetylcholine from the ileum. When all the calcium of Krebs solution had been replaced by strontium one-third of the control output of acetylcholine was obtained, but the smooth muscle of the guinea-pig ileum would not respond to drugs under these conditions. Strontium could thus partially substitute for calcium in nerves but not in muscle. Hemicholinium-3 (100 mug/ml.) inhibited the spontaneous release of acetylcholine and 400 mug/ml. of choline was required to reverse the inhibition. It is concluded that cocaine, procaine, cooling, reduction of calcium ion and increase of magnesium ion concentrations all reduce the spontaneous output of acetylcholine, which has its origin in the parasympathetic nerve-endings of the intramural nerve plexuses. Further, the hemicholinium experiments seem to justify the conclusion that the release of acetylcholine is reduced because synthesis is reduced.

Acetylcholine↗
PubMed1964

ACTIONS OF MECAMYLAMINE, DIMECAMINE, PEMPIDINE AND THEIR TWO QUATERNARY METHO-SALTS AT THE NEUROMUSCULAR JUNCTION.

Mecamylamine, dimecamine and pempidine differed in neuromuscular-blocking activity on the isolated phrenic nerve-diaphragm preparation of the rat from the corresponding methiodides by a factor of less than two. It was concluded that the active component of each amine was the cation acting extracellularly. The finding that the neuromuscular-blocking activity of mecamylamine at pH 6.7 was similar to the activity at pH 7.7 did not refute this conclusion. Mecamylamine, dimecamine methiodide, dimecamine and pempidine, at concentrations insufficient to cause block, could increase the twitch response of the rat diaphragm; the ability to do this increased in the above order. With pempidine (the most active compound) this effect, on the isolated sartorius muscle of the frog, was a direct action. During steady partial block by each of the compounds, the responses to brief tetanic stimulation, to neostigmine and to an increase in calcium concentration were similar to those observed during block by tubocurarine. From indirect evidence, pempidine methiodide appeared both to enhance the release of acetylcholine from motor-nerve terminals and to cause postsynaptic block.

Abdominal Muscles↗
PubMed1964

THE SELECTIVITY OF DRUGS BLOCKING GANGLIONIC TRANSMISSION IN THE RAT.

By comparing the effects on ganglionic transmission and on the pre- and post-ganglionic nerves in the isolated superior cervical ganglion preparation of the rat, the selectivity of several drugs was assessed quantitatively. Hexamethonium, tetraethylammonium, nicotine and tubocurarine blocked transmission in concentrations which did not affect nervous conduction and were considered to be highly selective in action. Atropine, amylobarbitone and paraldehyde depressed nervous conduction appreciably in ganglion-blocking doses, but not enough to account wholly for the block in transmission and they were therefore considered as being moderately selective. The ganglion blocking actions of mephenesin, procaine, methylpentynol, methylpentynol carbamate and benactyzine were nonspecific, showing general depression of neuronal activity. Ganglion block with bretylium was nonselective in its site of depression of the postganglionic neurone in concentrations which only partly depressed the preganglionic nerve.

Atropine↗
PubMed1964

THE SYMPATHETIC POSTGANGLIONIC FIBRE AND THE BLOCK BY BRETYLIUM; THE BLOCK PREVENTED BY HEXAMETHONIUM AND IMITATED BY MECAMYLAMINE.

Acetylcholine, in the presence of atropine, has an action like that of sympathetic stimulation. When injected into the splenic artery it causes contraction of the spleen, but this action is blocked by hexamethonium; stimulation of the splenic nerves, however, is still effective. Thus hexamethonium distinguishes between sympathetic nerve stimulation and the action of acetylcholine. If bretylium is used instead of hexamethonium, there is no such distinction, for bretylium blocks the response to nerve stimulation as well as that to acetylcholine. It appeared that hexamethonium might block the action of acetylcholine by preventing its entry into the sympathetic fibre. Acetylcholine has some structural similarity to bretylium, since acetylcholine is a derivative of trimethylammonium and bretylium is a derivative of dimethylethylammonium. It has been found that hexamethonium, pentolinium and hemicholinium (HC-3), which are all bis-quaternary compounds, block the action of bretylium, presumably by preventing its entry into the fibre. Consistent with the view that ability to enter the fibre is important is the observation that mecamylamine and pempidine, which are ganglion-blocking agents, but not either mono- or bis-quaternary compounds, often abolish the response to stimulation of the sympathetic postganglionic fibre.

Acetylcholine↗