Dexamethasone-Induced Increase in Lymphocyte β-Adrenergic Receptor Density and cAMP Formation in vivo

The influence of dexamethasone on the density of β 2 -adrenergic receptors (β 2 -adrenergic receptors (β 2 AR) and on the intracellular adenosine 3′,5′-cyclic monophosphate (cAMP) response was studied in equine lymphocytes in vivo. Dexamethasone (0.1 mg/kg/day, 1–5 days) raised the number of β 2 AR – B max as assessed by (–)-[ 125 I]iodocyanopindolol binding (ICYP) – to 2.5- to 3.5-fold as compared with control values. The increase in β 2 AR number was fast (342 ± 49 vs. 960 ± 103 binding sites/lymphocyte after 24 h), reaching a maximum between 48 and 96 h (342 ± 49 vs. 1,289 ± 150 and 1,106 ± 68 binding sites/lymphocyte, respectively). The isoprenaline-induced cAMP accumulation (measured by a [ 3 H]-cAMP radioimmunoassay system) was concomitantly enhanced by dexamethasone (1.5- to 2.4-fold). Both parameters were reversible to a similar rate at dexamethasone withdrawal. The changes in the functional responsiveness of lymphocytes were not reflected by changes in the binding affinity for ICYP of β 2 AR. These results demonstrate the in vivo glucocorticoid-mediated regulation of β 2 AR in equine lymphocytes which has already been suggested on the basis of in vitro observations in other tissues.