Die Wirkung von Cocain, Guanethidin, Reserpin, Hexamethonium, Tetracain und Psicain auf die Noradrenalin-Freisetzung aus dem Herzen

Lindmar, R.; Muscholl, E.

doi:10.1007/bf00246606

Cited by 66 publications

(22 citation statements)

References 27 publications

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“…Thus, tyramine caused a loss of adrenaline and noradrenaline from the toad heart and there was an increase in the amplitude and sometimes in the rate of beating. This cardiac stimulation is in accord with the observations made on the mammalian heart with tyramine (Lindmar & Muscholl, 1961 ;Davey & Farmer, 1963). Similarly, when the toad heart was exposed to phenoxybenzamine there was a considerable reduction in adrenaline and noradrenaline in the heart and the release of these catecholamines probably explains the stimulant actions of phenoxybenzamine on the isolated toad heart.…”

Section: Discussionsupporting

confidence: 88%

Temperature dependence of catecholamine depletion by reserpine in the heart of the toad (Bufo marinus)

Chang

Rand

1971

British J Pharmacology

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Summary1. The catecholamines in toad ventricle were adrenaline (90%) and noradrenaline (10%); there was no dopamine. 2. Phenoxybenzamine and tyramine stimulated the isolated heart and reduced the catecholamine content.3. Reserpine treatment of toads kept at 200 C did not affect the adrenaline but reduced the noradrenaline content of the ventricle. 4. At 370 C, reserpine caused depletion of both adrenaline and noradrenaline, and the stimulant actions of phenoxybenzamine and tyramine were lost.

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Section: Discussionsupporting

confidence: 88%

Temperature dependence of catecholamine depletion by reserpine in the heart of the toad (Bufo marinus)

Chang

Rand

1971

British J Pharmacology

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“…It may thus be assumed that tyramine not only displaces catechol amines from tissue stores but also interferes with their subsequent uptake. This could explain a similar " sensitizing " effect of tyramine observed by Lindmar & Muscholl (1961) with rabbit isolated perfused hearts, where the chronotropic effect of tyramine was greater than that of dimethylphenylpiperazinium at doses of each drug which released the same amount of noradrenaline. The antagonism of tyramine at tissue binding sites as well as at catechol amine receptors is a competitive one and rapidly disappears with repeated injections of noradrenaline.…”

Section: Discussionsupporting

confidence: 56%

“…Experiments published in the last two years have supplied direct proof for such an effect in vivo as well as in vitro (von Euler & Lishajko, 1960;Schumann & Weigmann, 1960;Lockett & Eakins, 1960;Schumann & Philippu, 1961;Lindmar & Muscholl, 1961;Carlsson & Hillarp, 1961;Cession-Fossion, 1962;Potter, Axelrod & Kopin, 1962;Chidsey, Harrison & Braunwald, 1962 ;Weiner, Draskoczy & Burack, 1962). Further evidence for this mode of action is provided by the fact that the sympathomimetic effect of tyramine on different effector organs (for example, arteries, heart, spleen, nictitating membrane and iris) can be reduced either by depleting stores of catechol amine (for example, by chronic denervation, treatment with reserpine or by tyramine itself) or by drugs (such as cocaine, guanethidine, bretylium and imipramine) which block the access of tyramine to catechol amine stores or to cells containing these stores (Schaeppi, 1960;Lindmar & Muscholl, 1961;Legic & Varagic, 1961;Axelrod, Gordon, Hertting, Kopin & Potter, 1962).…”

mentioning

confidence: 99%

The Responses to Tyramine of the Normal and Denervated Nictitating Membrane of the Cat: Analysis of the Mechanisms and Sites of Action

Haefely

Hürlimann

Thoenen

1963

British Journal of Pharmacology and Chemotherapy

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The response to tyramine of the denervated nictitating membrane has been analysed by comparing dose/response curves obtained by injections into the femoral vein and into the carotid artery of the spinal cat while recording contractions of innervated and chronically denervated membranes and those of cats treated with reserpine. It is concluded that the effect of tyramine given by these routes is due primarily to catechol amines released from stores within the nictitating membrane itself. Higher doses of tyramine also cause contraction of the membrane by liberating catechol amines into the circulating blood from stores outside the membrane. The response to tyramine of the nictitating membrane after chronic denervation and/or prior treatment with reserpine is partially due to catechol amines released from unidentified stores within the membrane which resist depletion by reserpine and by postganglionic denervation; evidence is presented that adrenaline rather than noradrenaline is concerned. Because of the high sensitivity of the denervated nictitating membrane to adrenaline and to noradrenaline, the response to these a-mines released from stores outside the membrane by intravenous injections of tyramine becomes greater than that of the normal membrane. Dose/response curves obtained from responses to intravenous sympathomimetic drugs which act away from the membrane are therefore not fully representative of the effect of the drugs on the membrane itself. Tyramine probably has an affinity both for storage sites and for catechol amine receptors in the smooth muscle of the nictitating membrane, the "intrinsic activity," however, being very weak or even absent.It is generally accepted that tyramine owes at least the main part of its sympathomimetic effect to the release of the normal sympathetic transmitter from stores within or in the vicinity of adrenergic nerve endings. Experiments published in the last two years have supplied direct proof for such an effect in vivo as well as in

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“…This is most likely to be a local anaesthetic action, which would oppose the depolarizing effects of nicotinic receptor stimulation by nonspecific stabilization of the neuronal cell membrane. Experimental evidence supporting such a mechanism has been provided by Lindmar & Muscholl (1961) and Westfall & Brasted (1972), who demonstrated inhibitory effects of local anaesthetic agents on the nicotine-evoked release of noradrenaline from cardiac sympathetic nerves. In the present study, cocaine, McN-A-343 and AHR 602 have all been shown to have local anaesthetic properties (Fig.…”

Section: Estimation Of Noradrenalinementioning

confidence: 92%

ATROPINE‐RESISTANT EFFECTS OF THE MUSCARINIC AGONISTS McN‐A‐343 AND AHR 602 ON CARDIAC PERFORMANCE AND THE RELEASE OF NORADRENALINE FROM SYMPATHETIC NERVES OF THE PERFUSED RABBIT HEART

Fozard

Muscholl²

1974

British J Pharmacology

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1 The effects of 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride and N-benzyl-3-pyrrolidyl 4 McN-A-343, cocaine and desipramine (but not AHR 602 or hexamethonium) blocked the net cardiac noradrenaline uptake and increased the positive chronotropic effect of noradrenaline. 5 Prior perfusion with concentrations of cocaine and desipramine sufficient to block uptake reduced or abolished the facilitatory effects of both McN-A-343 and AHR 602 on SNS. 6 Cocaine, McN-A-343 and AHR 602 displayed local anaesthetic properties on the guinea-pig wheal and frog nerve plexus tests, and their relative potencies in this respect were similar to those for inhibition of DMPP-evoked transmitter overflow. Hexamethonium did not produce local anaesthesia. 7 The results indicate that the facilitated release of noradrenaline after SNS and the inhibition of release after DMPP produced by McN-A-343 and AHR 602 are the result of their combined local anaesthetic action and inhibition of amine uptake.

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Die Wirkung von Cocain, Guanethidin, Reserpin, Hexamethonium, Tetracain und Psicain auf die Noradrenalin-Freisetzung aus dem Herzen

Cited by 66 publications

References 27 publications

Temperature dependence of catecholamine depletion by reserpine in the heart of the toad (Bufo marinus)

Temperature dependence of catecholamine depletion by reserpine in the heart of the toad (Bufo marinus)

The Responses to Tyramine of the Normal and Denervated Nictitating Membrane of the Cat: Analysis of the Mechanisms and Sites of Action

ATROPINE‐RESISTANT EFFECTS OF THE MUSCARINIC AGONISTS McN‐A‐343 AND AHR 602 ON CARDIAC PERFORMANCE AND THE RELEASE OF NORADRENALINE FROM SYMPATHETIC NERVES OF THE PERFUSED RABBIT HEART

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