EFFECT OF HYDROCORTISONE ON BETA-ADRENERGIC RECEPTORS IN LUNG MEMBRANES

被引：149
|
作者：
MANO, K [1 ]
AKBARZADEH, A [1 ]
TOWNLEY, RG [1 ]
机构：
[1] CREIGHTON UNIV, SCH MED, CTR ALLERG DIS, OMAHA, NE 68178 USA
来源：
LIFE SCIENCES | 1979年 / 25卷 / 22期
基金：
美国国家卫生研究院;
关键词：
D O I：
10.1016/0024-3205(79)90614-3
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Glucocorticoids potentiate .beta.-adrenergic stimulation of cardiovascular and airway tissues. The effect of glucocorticoids on the number and affinity of .beta.-adrenergic receptors in animal lung tissues was studied by a direct binding technique using 125I-iodohydroxybenzylpindolol (125I-HYP), a potent .beta.-adrenergic receptor antagonist. Specific binding of 125I-HYP to rat lung membranes was saturable with 386 f[femto]mol of 125I-HYP/mg protein at saturation. The apparent equilibrium Kd of 125I-HYP for .beta.-receptors was 221 nM. Chronic administration of hydrocortisone increased the density of .beta.-adrenergic receptors by 70% from 386-657 fmol/mg with some decrease in the affinity of 125I-HYP for .beta.-adrenergic receptors. Adrenalectomy produced a 29% fall in the number of .beta.-adrenergic receptors without altering the affinity of 125I-HYP for .beta.-receptors, and this change was reversed by exogenous administration of hydrocortisone. Apparently, glucocorticoids may participate in regulating the density of .beta.-adrenergic receptors and may potentiate .beta.-adrenergic receptor stimulation, by increasing .beta.-receptor density in tissue membranes.
引用
收藏
页码：1925 / 1930
页数：6
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