Adrenoceptors Beta-adrenergic receptor

VanDenMeiracker, A., Manln tVeld, A., Boomsma, F., Fischberg, D., Molinoff, P., and Schalekamp, M., Hemodynamic and beta-adrenergic receptor adaptations during long-term beta-adrenoceptor blockade. Studies with acebutolol, atenolol, pindolol, and propranolol in hypertensive patients, Circulation, Vol. 80, No. 4, 1989, pp. 903-914. 

To clarify some of the puzzling differential effects of sympathomimetic drugs on various tissues, in 1948 Ahlquist (76) introduced the concept of two distinct types of adrenergic receptors as defined by their responses to (1), (2), and (17), which he called alpha receptors and beta receptors. Alpha receptors were defined as those that responded in rank order of agonist potency as (2) > (1) (17). Beta receptors were defined as those responding in potency order of (17) > (2) > (1). Subsequently, /3-receptors were further divided into /3i-receptors, located primarily in cardiac tissue, and /32-adrenoceptors, located in smooth muscle and other tissues, given that (1) and (2) are approximately equipotent at cardiac... 

Sympathomimetics mimic the action of noradrenaline (norepinephrine), the principal neurotransmitter between the nerve endings of the sympathetic nervous system and the adrenergic receptors of the innervated tissues. They stimulate both alpha-adrenoceptors, causing constriction of smooth muscle and blood vessels, and beta-adrenoceptors, producing bronchodilatation. They are therefore useful in coughs where the tissues of the upper respiratory tract are congested, as they shrink swollen mucosa and open up the airways. 

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. 

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