TY - JOUR
T1 - Glucocorticoid modulation of β-adrenergic receptors of cultured rat arterial smooth muscle cells
AU - Jazayeri, A.
AU - Meyer, W. J.
PY - 1988
Y1 - 1988
N2 - Since both glucocorticoids and catecholamines are involved in the regulation of normal blood pressure, we investigated the modulation of β-adrenergic receptors of cultured rat arterial smooth muscle cells by glucocorticoids. The synthetic glucocorticoids dexamethasone and RU 28362, at 10-8 M concentration, increased maximum β-adrenergic binding but had no effect on the dissociation constant (K(d)). Each steroid caused an increase in maximum [3H]dihydroalprenonol binding over the concentration range of 10-8 to 10-6 M, but not at 10-9 M. The glucocorticoid effect on β-adrenergic receptors of arterial smooth muscle cells required a minimum of 20 hours of incubation in the presence of the steroid and was significantly inhibited by cycloheximide (10 μg/ml), indicating that the glucocorticoid effect required protein synthesis. The effect of dexamethasone on [3H]dihydroalprenolol binding was significantly inhibited by the glucocorticoid antagonist RU 38486. Basal and agonist-stimulated cyclic adenosine 3',5'-monophosphate (cAMP) levels in arterial smooth muscle cells, before and after glucocorticoid treatment, were measured as an indicator of the physiological significance of the observed glucocorticoid-induced increase in β-adrenergic receptor binding. While causing no change in the basal cAMP level, treatment of arterial smooth muscle cells with 10-6 M dexamethasone for 24 hours increased the 10-6 M isoproterenol-stimulated cAMP levels.
AB - Since both glucocorticoids and catecholamines are involved in the regulation of normal blood pressure, we investigated the modulation of β-adrenergic receptors of cultured rat arterial smooth muscle cells by glucocorticoids. The synthetic glucocorticoids dexamethasone and RU 28362, at 10-8 M concentration, increased maximum β-adrenergic binding but had no effect on the dissociation constant (K(d)). Each steroid caused an increase in maximum [3H]dihydroalprenonol binding over the concentration range of 10-8 to 10-6 M, but not at 10-9 M. The glucocorticoid effect on β-adrenergic receptors of arterial smooth muscle cells required a minimum of 20 hours of incubation in the presence of the steroid and was significantly inhibited by cycloheximide (10 μg/ml), indicating that the glucocorticoid effect required protein synthesis. The effect of dexamethasone on [3H]dihydroalprenolol binding was significantly inhibited by the glucocorticoid antagonist RU 38486. Basal and agonist-stimulated cyclic adenosine 3',5'-monophosphate (cAMP) levels in arterial smooth muscle cells, before and after glucocorticoid treatment, were measured as an indicator of the physiological significance of the observed glucocorticoid-induced increase in β-adrenergic receptor binding. While causing no change in the basal cAMP level, treatment of arterial smooth muscle cells with 10-6 M dexamethasone for 24 hours increased the 10-6 M isoproterenol-stimulated cAMP levels.
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U2 - 10.1161/01.HYP.12.4.393
DO - 10.1161/01.HYP.12.4.393
M3 - Article
C2 - 2844667
AN - SCOPUS:0023727612
SN - 0194-911X
VL - 12
SP - 393
EP - 398
JO - Hypertension
JF - Hypertension
IS - 4
ER -