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  • Title: Lack of modulation by presynaptic alpha 2-adrenoceptors of adrenergic transmitters release evoked by activation of 5-hydroxytryptamine and nicotine receptors.
    Author: Carr SR, Fozard JR.
    Journal: Eur J Pharmacol; 1981 Jun 10; 72(1):27-34. PubMed ID: 6266849.
    Abstract:
    Clonidine (4.3 X 10(-6) M) and yohimbine (2.8 X 10(-6) M) have been used to stimulate and to block alpha 2-adrenoceptors in the isolated perfused rabbit heart. Transmitter release from the terminal sympathetic fibres as a result of stimulation of the nerves leaving the stellate ganglion (SNS; 0.32-10 Hz) and bolus injections of 5-hydroxytryptamine (5-HT; 2.8-182 nmol) or dimethylphenylpiperazinium (DMPP; 26-418 nmol) was estimated from changes in the chronotropic response of the heart under conditions of constant end organ sensitivity to injected noradrenaline (0.06-15.1 nmol). In accordance with the literature, clinidine inhibited responses to SNS and was more effective against low than against high frequencies of stimulation; similarly, yohimbine enhanced responses to SNS. In contrast, neither clonidine no yohimbine had any effect on the indirect sympathomimetic response to 5-HT. Similarly yohimbine did not alter responses to DMPP. Clonidine produced inconsistent effects on the response to DMPP; the response to 105 nmol was unchanged whereas the response to 209 nmol was reduced. The results suggest that transmitter release from the cardiac sympathetic nerves of the rabbit heart evoked by 5-HT or DMPP is not subject to control through activation of alpha 2-adrenoceptors by the released transmitter. They lend support to the suggestion of Stjärne that alpha 2-adrenoceptor inhibition of transmitter release arises primarily from the suppression of impulse transmission from varicosity to varicosity within the adrenergic ground plexus rather than interference with a Ca2+-dependent step in excitation-secretion coupling.
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