Summary
The hypothesis that in hypoglycaemia adrenoceptor-blocking drugs may enhance those metabolic effects of the catecholamines that remain unblocked has been investigated in 12 volunteers.
α-Adrenoceptor blockade with urapidil increased the heart rate and the plasma noradrenaline level, and increased the β-adrenoceptor mediated cellular uptake of potassium and phosphate, and the production of lactate. Posthypoglycaemic glucose intolerance and the counterregulatory responses of hGH and cortisol remained unchanged. Plasma adrenaline, the α-adrenoceptor mediated responses of cortisol and hGH, and the diastolic blood pressure were increased by propranolol.
Adrenoceptor blocking drugs produce an indirect stimulatory effect by eliciting a reflex increase in sympathetic tone, which is manifested as stimulation of receptors of the type that has not been blocked.
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Petersen, K.G., Katschker, P. & Kerp, L. Modulation of catecholamine effects during hypoglycaemia in man by urapidil and propranolol. Eur J Clin Pharmacol 36, 351–355 (1989). https://doi.org/10.1007/BF00558294
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DOI: https://doi.org/10.1007/BF00558294