1. The aim of the present study was to evaluate the metabolic responses produced in man by the β-adrenoceptor agonist BRL 35135, and to determine which of these responses are β3-, rather than β1- or β2-, mediated.

2. Eight normal male subjects received single oral doses of BRL 35135 (8 mg) or the selective β2-adrenoceptor agonist salbutamol (8 mg) after pretreatment with placebo, bisoprolol (5 mg) as a selective β1-antagonist or nadolol (20 mg) to block β1-and β2-, but not β3-adrenoceptors.

3. BRL 35135 and salbutamol produced a significant fall in serum potassium concentration compared with placebo, in keeping with β2-adrenoceptor stimulation. Both drugs also produced a significant increase in serum glucose, insulin and lactate concentrations, which mirrored the hypokalaemic response, being unaffected by selective β1-blockade (bisoprolol), but completely blocked by nadolol. BRL 35135 (but not salbutamol) also produced a significant rise in serum free fatty acid and glycerol concentrations, which appeared to be β2-mediated.

4. A significant increase in basal metabolic rate occurred with both BRL 35135 and salbutamol. In the case of salbutamol, this effect appeared to be mediated solely by β2-adrenoceptors, whereas BRL 35135 produced a thermogenic response which could only be partially accounted for by a combination of β1- and β2-adrenoceptor stimulation.

5. These results infer the possibility of thermogenic β3-adrenoceptors in man, although these do not appear to be involved in the control of carbohydrate or fat metabolism.

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