1. 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 20 degrees C did not affect the adrenaline but reduced the noradrenaline content of the ventricle.4. At 37 degrees C, reserpine caused depletion of both adrenaline and noradrenaline, and the stimulant actions of phenoxybenzamine and tyramine were lost.

Adrenergic Agents↗

PubMed1971

Effects of the muscarinic agonist McN-A-343 on responses to sympathetic nerve stimulation in the rabbit ear artery.

1. Observations were made on the effects of 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride (McN-A-343) on responses of isolated segments of the central artery of the rabbit's ear to sympathetic nerve stimulation and noradrenaline.2. With low frequencies of nerve stimulation (2-5 Hz), McN-A-343 caused a decrease in responses to sympathetic nerve stimulation. This effect of McN-A-343 was abolished by dexamphetamine or atropine. In the presence of atropine, McN-A-343 caused an increase in responses to sympathetic nerve stimulation.3. With high frequencies of nerve stimulation (10-20 Hz), McN-A-343 caused an increase in responses. This effect was not qualitatively changed in the presence of atropine.4. When McN-A-343 had an inhibitory effect on responses to sympathetic nerve stimulation, responses to noradrenaline were unaffected.5. It is suggested that McN-A-343 acts on muscarinic receptors through which noradrenaline release may be inhibited; it may also act on the cholinergic stage in adrenergic transmission postulated by Burn & Rand (1959).

Animals↗

PubMed1971

Facilitation of noradrenaline uptake by lithium.

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Animals↗

PubMed1970

The effects of cholinomimetic drugs on responses to sympathetic nerve stimulation and noradrenaline in the rabbit ear artery.

1. The effects of infusions of the cholinomimetic drugs acetylcholine, methacholine, muscarine, carbachol, arecoline and pilocarpine were examined on vasoconstrictor responses of the perfused rabbit ear artery to sympathetic nerve stimulation and to injections of noradrenaline.2. The first effect of very low concentrations of acetylcholine or muscarine was a slight enhancement of responses to sympathetic nerve stimulation, but when higher concentrations of acetylcholine, methacholine, muscarine, carbachol and arecoline were infused, these vasoconstrictor responses were decreased. With still higher concentrations the responses tended to increase in size during the infusion. After stopping an infusion, the depressed vasoconstrictor responses rapidly recovered and became enhanced.3. Infusions of pilocarpine in a wide range of concentrations generally caused enhancement of responses.4. The depressant effects of cholinomimetic drugs on the responses to sympathetic nerve stimulation were antagonized by atropine. Larger concentrations of the drugs overcame the blockade by atropine.5. The effects of acetylcholine, methacholine and muscarine on the responses to sympathetic nerve stimulation were more pronounced at low than at high frequencies of stimulation.6. Vasoconstrictor responses to injected noradrenaline were enhanced by acetylcholine or methacholine, whereas responses to sympathetic nerve stimulation were decreased by the same concentrations of these choline esters.7. It is suggested that cholinomimetic drugs may act on receptor sites associated with the adrenergic terminal axon and that they may facilitate or impair the release of noradrenaline and impair noradrenaline uptake.

Acetylcholine↗

PubMed1970