To (β) block or better block?BMJ 1995; 311 doi: https://doi.org/10.1136/bmj.311.7007.701 (Published 16 September 1995) Cite this as: BMJ 1995;311:701
- Morris J Brown
- Professor of clinical pharmacology Clinical Pharmacology Unit, University of Cambridge, Addenbrooke's Hospital Cambridge CB2 2QQ
β1 selectivity rarely matters in clinical practice despite the hype
Scarcely a week now passes without a new receptor subtype being described on which either endogenous neurotransmitters or hormones might act, usually as agonists, and which are rapidly proposed as novel targets for drugs, usually as antagonists. It is therefore ironic, but instructive, to recognise the debate that still stirs among doctors and pharmacologists over the relative merits of β1 selective and non-selective β blockade after more than 20 years' use in angina and hypertension.
The most recent airing of the debate concerned the paradoxical pressor response to non-selective β blockade.1 2 In the absence of β blockade, acute rises in circulating adrenaline concentrations hardly affect mean blood pressure because of opposing actions on systolic and diastolic blood pressure. The rise in systolic blood pressure is due mainly to vasoconstriction mediated by (α) adrenoceptors, and this is unopposed when a non-selective β blocker like propranololprevents the vasodilatation mediated by β2 adrenoreceptors. But two obstacles exist to concluding that selective β1 blockade must automatically be preferable.
Firstly, it is necessary to appreciate that the endocrine secretion …
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