Abstract
Neurotransmitters and drugs interact with specific receptors in order to produce a cellular response. This recognition of specific agonists by receptors is the first step in an amplification process resulting in physiological modulation of homeostasis. The concept of a receptor-mediated mechanism for drug action was first proposed by Langley (1878, 1905). In 1906, examination by Dale of the action of various ergot alkaloid compounds in physiological preparations led to the observation of a number of compounds which would inhibit the excitatory effects of epinephrine without affecting its inhibitory actions. These types of observations provided support for the earliest notions of specific sites for catecholamine receptor interactions. In 1948, Ahlquist categorically demonstrated using a series of several sympathomimetic amines one order of potency in stimulating vasoconstriction and excitation of the uterus and ureters, and a different order of potency for these compounds for stimulation of vasodilation, for inhibition of uterine tone, and for stimulation of the heart. Ahlquist (1948) proposed that these actions of catecholamines were in fact mediated by two distinct populations of receptors which he termed α and β, and that in many cases, both receptors are present in the same organ or tissue. This proposal of distinct populations of adrenergic receptors has been strongly supported by the synthesis of a large number of potent agonists and antagonists that are clearly specific for α- or β- receptor-mediated functions. More recent pharmacological studies have resulted in the further subclassification of these α- and β-receptors.
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Shorr, R.G.L., Lefkowitz, R.J., Caron, M.G. (1985). The β-Adrenergic Receptor:Elucidation of Its Molecular Structure. In: Martonosi, A.N. (eds) The Enzymes of Biological Membranes. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2355-6_12
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