Abstract
The development during the 1960s of drugs which specifically antagonise β-adrenoceptors has led to the introduction of a new class of therapeutic agents of established value in the treatment of a variety of cardiovascular diseases, including angina, cardiac arrhythmia and hypertension. It has been assumed that these effects are mediated primarily by the antagonism of the effects of noradrenaline at receptor sites within the peripheral autonomic nervous system. In hypertension, however, the mode of action is by no means certain, and evidence has been put forward in support of a centrally mediated component (Day and Roach, 1973). Various central nervous system effects have been noted in both animals and man, and these effects may provide a basis for the claimed therapeutic benefits seen in some psychiatric and neurological disorders. The mechanisms underlying these therapeutic claims are poorly understood, since β-adrenoceptor antagonists have pharmacological actions other than at β-adrenoceptors and the role of the latter in the CNS is unknown.
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References
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Buxton, D.A., Greenwood, D.T., Middlemiss, D.N. (1982). Central Nervous Actions of Beta-Adrenoceptor Antagonists. In: Hoffmeister, F., Stille, G. (eds) Psychotropic Agents. Handbook of Experimental Pharmacology, vol 55 / 3. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67770-0_16
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