The inhibition of adrenaline oxidation by local anaesthetics

Philpot, Flora J.

doi:10.1113/jphysiol.1940.sp003808

Cited by 55 publications

(13 citation statements)

References 8 publications

(2 reference statements)

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“…However, the potentiation of tryptamine and 5-hydroxytryptamine by cocaine remains unexplained. It does not appear to be due to inhibition of monoamine oxidase by cocaine (Philpot, 1940), since inhibition of this enzyme potentiates tryptamine but not 5-hydroxytryptamine (Vane, 1959), whereas cocaine potentiated both amines to the same extent.…”

Section: Discussionmentioning

confidence: 89%

Some Cocaine‐like Actions of 3‐phenoxypropylguanidine

Bartlet

1962

British Journal of Pharmacology and Chemotherapy

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In anaesthetized cats 3-phenoxypropylguanidine caused a contracture of the nictitating membrane, a dilatation of the pupil and a fall followed by a rise in the arterial blood pressure. In spinal preparations of cats the initial fall in blood pressure was usually absent and the rise in blood pressure subsided to a steady level, which was about 10 mm Hg above the initial pressure. The pressor action and the contracture of the nictitating membrane were inhibited by phenoxybenzamine and by previous treatment with reserpine, but were not abolished by adrenalectomy and bretylium. 3-Phenoxypropylguanidine potentiated the actions of adrenaline and noradrenaline, increased the blood glucose concentration of the rabbit and decreased the appetite of the cat. The action of tyramine on the cardiovascular system was inhibited by 3-phenoxypropylguanidine, but the stimulant action of tyramine on the nictitating membrane of the cat was not abolished by this substance. Although 3-phenoxypropylguanidine produced a local anaesthesia of long duration in guineapig skin, it failed to anaesthetize the rabbit cornea. The responses to stimulation of the preganglionic cervical sympathetic nerve of the cat and the great auricular nerve of the rabbit ear were not abolished by 3-phenoxypropylguanidine; neither did this substance abolish the nicotinic action of acetylcholine in atropinized cats. Contractions of the rat fundus to tryptamine and 5-hydroxytryptamine were antagonized by 3-phenoxypropylguanidine, but were potentiated by cocaine.When reserpine is administered to a mouse, the eyes become closed. This may be due to the disappearance of catechol amines and 5-hydroxytryptamine from the mouse; since when these amines reappear, as after administration of their aminoacid precursors, the eyes are reopened (Carlsson, Lindqvist & Magnusson, 1957). The eyes of the reserpinized mouse are also reopened by the administration of 3-phenoxypropylguanidine (Chen, unpublished observation), and this suggested that this substance might potentiate the action of one of these amines. The experiments to be described showed that this was the case; adrenaline and noradrenaline were potentiated by 3-phenoxypropylguanidine, although 5-hydroxytryptamine was antagonized. The examination of 3-phenoxypropylguanidine in more detail revealed a most striking pharmacological resemblance to cocaine.

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Section: Discussionmentioning

confidence: 89%

Some Cocaine‐like Actions of 3‐phenoxypropylguanidine

Bartlet

1962

British Journal of Pharmacology and Chemotherapy

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“…As was to be expected, ecgonine did not have the effect of cocaine. The effect of other local anaesthetics The local anaesthetics other than cocaine which were used in this investigation all inhibited amine oxidase in vitro (Philpot, 1940). The only one with an effect similar to that of cocaine was amylocaine HCI (Stovaine) although the doses required (20 mg/kg or more) were much larger than those of cocaine.…”

Section: Resultsmentioning

confidence: 95%

The action of sympathomimetic amines on the rate of the denervated heart of the cat

Innes¹,

Kosterlitz²

1954

The Journal of Physiology

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“…Burn & Robinson (1952) found that the amine oxidase content of the nictitating membrane falls after denervation. On the strength of this finding and the fact that cocaine inhibits amine oxidase (Philpot, 1940), they formulated their theory that the changes caused by denervation or cocaine are due to a loss or inhibition of amine oxidase. In view of the general rise in sensitivity to sympathomimetic amines which is found after decentralization of the nictitating membrane, it would be of interest to know what happens to the amine oxidase content of such membranes.…”

Section: Discussionmentioning

confidence: 99%