Adrenergic receptors: Possible mechanism of inverse regulation of α- and β-receptors
Many physiologic and pathologic conditions, including bronchial asthma, are associated with inverse changes in α- and β-receptor-mediated responses in various tissues. The direction of the change elicited by a given stimulus is tissue specific, as exemplified by the actions of thyroid hormones: In t...
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Published in | Journal of Allergy and Clinical Immunology [J. ALLERGY CLIN. IMMUNOL.]. Vol. 76, no. 2 pt. 2. 1985 Vol. 76; no. 2; pp. 346 - 351 |
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Main Authors | , , , |
Format | Journal Article Conference Proceeding |
Language | English |
Published |
United States
Mosby, Inc
01.08.1985
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Subjects | |
Online Access | Get full text |
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Summary: | Many physiologic and pathologic conditions, including bronchial asthma, are associated with inverse changes in α- and β-receptor-mediated responses in various tissues. The direction of the change elicited by a given stimulus is tissue specific, as exemplified by the actions of thyroid hormones: In the rat heart, hypothyroidism reduces β- and increases α-receptor responses, whereas in the rat liver it has the opposite effects. A similar increase in β- and decrease in α-receptor responses in the rat liver is triggered by a number of different conditions, including glucocorticoid deficiency, that appear to represent lower levels of cellular differentiation. Among these, incubation of isolated hepatocytes in a serum-free buffer triggers the conversion of the receptor response in vitro within 4 hours, without parallel changes in the density or affinity of receptor binding sites. This change can be acutely reversed by an endogenous inhibitor of membrane phospholipase A
2, or accelerated by an activator of phospholipase A
2, suggesting that changes in the activity of this enzyme are involved in the conversion of the hepatic adrenoceptor response. The glucocorticoid-induced increase in β-receptors in cultured human lung adenocarcinoma cells also appears to be mediated indirectly through the induction of an endogenous inhibitor (lipomodulin) of membrane phospholipase A
2. The possible relevance of altered membrane phospholipid metabolism in the pathomechanism of asthma and in the associated glucocorticoid-sensitive changes in adrenergic receptor mechanisms is discussed. |
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Bibliography: | SourceType-Books-1 ObjectType-Book-1 content type line 25 ObjectType-Conference-2 SourceType-Conference Papers & Proceedings-2 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0091-6749 1097-6825 |
DOI: | 10.1016/0091-6749(85)90652-9 |