Adrenergic stimulation 3-Adrenoceptor antagonist

Class II catecholamine blockade. Propranolol and other p-adrenoceptor antagonists reduce background sympathetic tone in the heart, reduce automatic discharge (phase 4) and protect against adrenergically stimulated ectopic pacemakers. 

Beta-adrenoceptor antagonists are used in the treatment of hyperthyroidism to alleviate symptoms but are not considered to influence thyroid hormone production nor the effect of the hormone on cell function. A study of the effect of beta-blockers on lymphocyte metabolism was done with the purpose to clarify their mechanism of action in hyperthyroidism [68]. When hyperthyroid subjects were treated with beta-blockers, lymphocyte heat production was found to be within normal limits, thus showing that beta-blockers prevent the expected increased of cell metabolism under stimulation of thyroid hormone. These results seem to indicate that increased thermogenesis in hyperthyroidism is mediated via adrenergic receptors, rather than via nuclear thyroid hormone receptors. 

Early evidence that prejunctional histamine H3-receptors may modulate the sympathetic nerve activity on the heart was provided by Luo et al., (1991). These authors clearly stated that the selective H3-agonist (R)a-methylhistamine attenuates the inotropic response induced by transmural stimulation of the adrenergic nerve terminals in the isolated right atrium, without affecting basal contractile force of the preparation or the positive inotropic effect elicited by exogenous noradrenaline. The effect of (R)a-methylhistamine, which is not modified by Hi and H2-receptor blockade, was reversed by the specific H3-receptor antagonist thioperamide, at concentrations which do not influence the inhibitory activity mediated by other presynaptic receptors, like a2-adrenoceptors. 

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