Parker C W, Baumann M L, Huber M G
J Clin Invest. 1973 Jun;52(6):1336-41. doi: 10.1172/JCI107305.
In an effort to clarify the basis for the reduced cyclic AMP response to catecholamines in leukocytes and lymphocytes from asthmatic donors the response of these cells to prostaglandins has been examined. Cells with an impaired beta adrenergic response had an essentially unaltered response to prostaglandin E(1) (PGE(1)) indicating the presence of selective beta adrenergic blockade. In contrast to what was observed with cells from asthmatic individuals, in normal control leukocytes with reduced catecholamine responsiveness PGE(1) responses were usually reduced as well, suggesting a different mechanism. The excellent cyclic AMP response to PGE(1) in cells from asthmatic donors would suggest that the defect in catecholamine responsiveness is at the level of the beta adrenergic receptor although a contributory role of altered substrate concentrations or increased phosphodiesterase activity is not formally excluded.
为了阐明哮喘患者供体的白细胞和淋巴细胞中对儿茶酚胺的环磷酸腺苷(cAMP)反应降低的基础,已对这些细胞对前列腺素的反应进行了研究。β肾上腺素能反应受损的细胞对前列腺素E1(PGE1)的反应基本未改变,表明存在选择性β肾上腺素能阻断。与哮喘个体的细胞观察结果相反,在儿茶酚胺反应性降低的正常对照白细胞中,PGE1反应通常也降低,提示机制不同。哮喘患者供体细胞对PGE1有良好的cAMP反应,这表明儿茶酚胺反应性缺陷在于β肾上腺素能受体水平,尽管底物浓度改变或磷酸二酯酶活性增加的辅助作用并未被完全排除。