1. Adrenoceptor subtype function was studied in isolated adipocytes obtained by subcutaneous fat biopsies from nine patients with mild asthma. The biopsies were taken before and after 7 days treatment with 25 mg of prednisolone given orally. Lipolytic activity after stimulation with various adrenergic agents was measured, using glycerol release as an index of lipolysis. The number of β1- and β2-adrenoceptor binding sites was determined in radioligand binding experiments and β1- and β2-adrenoceptor mRNA levels were measured with a solution hybridization assay.

2. Lipolytic sensitivity (ED50) to isoprenaline, a nonselective β-adrenoceptor agonist, increased 50-fold after treatment (P = 0.04). Sensitivity to terbutaline, a selective β2-adrenoceptor agonist, increased 25-fold (P =0.01), whereas the ED50 values for dobutamine, a selective β1-adrenoceptor agonist, did not change significantly. Likewise, the sensitivity to the α2-adrenoceptor agonist, clonidine, and to the drugs acting at post-receptor levels did not change significantly. Basal and maximum lipolytic rates on stimulation were not altered by the treatment.

3. The number of β2-adrenoceptor binding sites increased by 60% after treatment (P <0.05), whereas the β1-adrenoceptor binding sites were not affected. The affinity of each receptor subtype for the displacing ligand, ICI 118.551, was not significantly altered by steroids. No significant changes were demonstrated in either β1- or β2-adrenoceptor mRNA levels.

4. Thus, glucocorticoids selectively increase β2-adrenoceptor density and function in patients with asthma, studied by using subcutaneous fat cells as an experimental model.

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