The effect of inhibition of amine oxidase <i>in vivo</i> on administered adrenaline, noradrenaline, tyramine and serotonin

Corne, S. J.; Graham, J. D. P.

doi:10.1113/jphysiol.1957.sp005714

Cited by 68 publications

(7 citation statements)

References 14 publications

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“…These substances were chosen because of their apparent potency and because others like ephedrine which have an affinity for the same receptors as the transmitter could not be used as they might act in the same way as dibenzyline. The ability of iproniazid to penetrate cells has been questioned by Udenfriend, Weissbach & Bogdanski (1957), who attribute to this property their failure to demonstrate any activity of this substance in vivo, although Koelle & Valk (1954) and Corne & Graham (1957) did obtain evidence of its power to penetrate cells. It seems unlikely that both choline-p-tolyl ether and propamidine should be ineffective for the same reason, and this applies with particular force to propamidine which NORADRENALINE FROM INTESTINES is a powerful liberator of histamine and probably acts, therefore, within the cell.…”

Section: Discussionmentioning

confidence: 99%

The release of chemical transmitter from the sympathetic nerves of the intestine of the cat

Brown¹,

Davies²,

Gillespie³

1958

The Journal of Physiology

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In a previous paper (Brown & Gillespie, 1957) we have shown that the noradrenaline released when the sympathetic nerve supply to the spleen is stimulated can be estimated in the venous blood leaving the organ. The maximum output per stimulus occurred at frequencies of 30/sec. Administration to the animal of substances blocking the effect of the liberated transmitter on the innervated cells increased the output of noradrenaline at frequencies below 30/sec.These experiments were made on the spleen of the cat because it was the only tissue from which we could regularly obtain amounts of transmitter sufficient for an adequate assay. From the colon of the cat and the ear of the rabbit, for instance, we could obtain either no transmitter at all or amounts at the lower limit of detectability. The spleen, however, has certain disadvantages as a tissue for these experiments; the circulation of blood through it is complex and obscure, stimulation of the nerves causes an expulsion of stored red cells, and this effect is absent after a blocking agent has been administered. All these factors might influence the appearance of liberated transmitter in a venous sample, without necessarily reflecting changes in the amount liberated or destroyed in the vicinity of the nerve endings.We have accordingly re-investigated the intestines in the light of the information we obtained from the spleen. The administration of a sympathetic blocking agent has again been found to increase the amounts of transmitter detectable in the venous blood. Three substances to which anti-amine oxidase activity has been attributed were found to be without effect on the output of transmitter. Additional information has been obtained about the factors governing the release and appearance of the sympathetic transmitter.

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Section: Discussionmentioning

confidence: 99%

The release of chemical transmitter from the sympathetic nerves of the intestine of the cat

Brown¹,

Davies²,

Gillespie³

1958

The Journal of Physiology

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“…The present results showed that the junction potentials were depressed by inhibition of MAO. However, the depressive effect of MAO inhibition on adrenergic transmission at the level of the postsynaptic membrane is not unusual, since a few inves tigators have demonstrated that inhibition of MAO failed to potentiate the action of noradrenaline administered exogenously or released by nerve stimulation (11,15). In hibition of the enzyme also does not increase the out-flow of noradrenaline from cat spleen during sympathetic nerve stimulation (12).…”

Section: Discussionmentioning

confidence: 99%

Effects of Enzyme Inhibitors on Junction Potentials in Response to Adrenergic Nerve Stimulation

Nakanishi

Doteuchi

Otani

et al. 1969

Japanese Journal of Pharmacology

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Recent electrophysiological and anatomical studies on transmission between the sympathetic nerve and smooth muscle have confirmed the important role of a chemical substance acting in a manner similar to the chemical substance concerned with transmis sion between somatic nerve and skeletal muscle. A low frequency stimulation of the hypogastric nerve produced junction potentials on the smooth muscle of the vas deferens (1) and seminal vesicle (2) in the guinea-pig. The junction potentials may be due to the release of noradrenaline from the sympathetic nerve terminals, and this conjecture is sup ported by the following evidence. 1) The junction potentials were strongly depressed by pretreatment or intravenous injection of reserpine (3, 4), 2) The junction potentials were also depressed by guanethidine, bretylium and high doses of various "-blocking agents , such as phenoxybenzamine, phentolamine and yohimbine (5), 3) The intravenous injection of noradrenaline induced a burst of action potentials in smooth muscle which was associated with tetanic contraction (6), 4) Many investigators (7,8) have demonstrated pharmaco logically that the nature of the contractile response of the vas deferens to hypogastric nerve stimulation was probably of sympathetic origin, 5) The guinea-pig vas deferens and seminal vesicle contain a large amount of noradrenaline and also abundant nor adrenaline containing fibers which have been observed among the smooth muscle cells (9, 10).On the other hand, it is well known that monoamine oxidase (MAO) and catechol O-methyl transferase (COMT) degrade noradrenaline to deaminated and methylated metabolites. However, there are a few inconsistent results concerning the effect of MAO inhibitor on the contractile response of the guinea-pig vas deferens to hypogastric nerve stimulation. For instance, Kamijo et al. (11) and Brown and Gillespie (12) have assumed that MAO inhibitors do not potentiate the effect of catecholamine released by nerve stimu lation, whereas Bhargava et al. (13) have observed that MAO inhibitors , such as pheni prazine and tranylcypromine, and a COMT inhibitor, pyrogallol, potentiated the con tractile response of the guinea-pig vas deferens to hypogastric nerve stimulation .The present study was, therefore, undertaken to examine the effect of inhibition of monoamine oxidase and catechol-O-methyl transferase on the junction potential recorded from the guinea-pig seminal vesicle in response to hypogastric nerve stimulation. METHODSMale guinea-pigs, weighing 350 to 450 g, were anesthetized by intraperitoneal in jection of NembutalR (35 mg/kg, sodium pentobarbital). Histochemistry: Both seminal vesicles were removed and small pieces of tissue were immediately frozen in a mixture of n-hexane and solid CO,. These were dried in vacuo at a temperature between -25 and -35°C for 7 days. After return to room tem perature, the dried tissue was incubated in formaldehyde vapour at a temperature of 80'C for one hour, which produced fluorescent substances from primary catecholamine such as nora...

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“…This possibility was investigated by studying the effect of an inhibitor of monoamine oxidase on the output of sympathin at 10 and 30/sec. isoNicotinylisopropyl hydrazine (iproniazid, Marsilid, Roche Products) was given intravenously in amounts known to inhibit monoamine oxidase (Corne & Graham, 1957). No difference was found in the output of noradrenaline before and after Marsilid at either frequency.…”

Section: Effect Of the Frequency Of Stimulation On Outputmentioning

confidence: 99%

The output of sympathetic transmitter from the spleen of the cat

Brown¹,

Gillespie²

1957

The Journal of Physiology

390

156

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The effect of inhibition of amine oxidase in vivo on administered adrenaline, noradrenaline, tyramine and serotonin

Cited by 68 publications

References 14 publications

The release of chemical transmitter from the sympathetic nerves of the intestine of the cat

The release of chemical transmitter from the sympathetic nerves of the intestine of the cat

Effects of Enzyme Inhibitors on Junction Potentials in Response to Adrenergic Nerve Stimulation

The output of sympathetic transmitter from the spleen of the cat

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