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β‐BLOCKERS and BLOOD SUGARS

Catecholamines mediate sympathetic activity throughout the body and, since carbohydrate metabolism is under sympathetic control they influence the availability of glucose for utilization as energy. They achieve this by modifying the response to a raised blood sugar by either suppressing insulin release, an a‐receptor stimulant effect, or by promoting insulin release, probably a β2 stimulant effect. When the blood sugar falls, catecholamines initiate metabolic processes which increase blood glucose and restore it to normal. This is also thought to be a β2‐receptor stimulant effect. It would therefore be expected that drugs which blocked β‐adrenoreceptors would interfere with both the insulin release which occurs during hyperglycaemia and the glycogenosis and gluconeogenesis which occur in response to a fall in blood sugar. Both of these actions have been demonstrated in acute studies usually in volunteers. The clinical relevance of these effects remains to be determined though some guidelines can be suggested on the basis of data currently available, and are given at the end of the paper.