![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
P Valet, JL Montastruc, M Berlan, MA Tran, M Lafontan and P Montastruc
Institut National de la Sante et de la Recherche Medicale Unite 317, Toulouse, France.
The effects of long-term endogenous catecholamine exposure on the regulation of leukocyte and adipocyte beta adrenoceptor subtypes were studied through an experimental model of chronic neurogenic hypertension in the dog. Chronic sinoaortic denervation (SAD) is associated with a significant increase in plasma catecholamine levels, a reduction in the total beta adrenoceptor number of the leukocytes (52%) as well as of the omental adipocytes (59%). Using highly selective beta antagonists (bisoprolol for beta-1; ICI 118,551 for beta- 2 adrenoceptors) we demonstrate that the normal dog fat cell possess both beta-2 and beta-1 adrenoceptors in proportions of 67 and 33%, respectively. SAD-induced catecholamine enhancement promotes a strong reduction of beta-2 (but not beta-1) adrenoceptor number (from 237 +/- 28 to 52 +/- 13 fmol/mg of protein) leading to a new relative distribution in fat cell membranes: 36% for beta-2 and 64% for beta-1 adrenoceptors. Such a different regulation provokes major consequences in the associated-biological effect on adipocytes when evaluating the lipolytic process. Lipolysis induced by epinephrine or isoproterenol (two mixed agonists) is weakly but significantly reduced whereas lipolysis induced by procaterol (a highly selective beta-2 agonist) is strongly reduced. These data fit with the results of the binding studies and demonstrate the loss in beta-2 adrenoceptor number and efficiency in SAD dogs. The present study demonstrates a differential regulation of beta adrenoceptors: beta-2 but not beta-1 adrenoceptors are decreased by long-term exposure to high plasma levels of endogenous catecholamines in the dog.
This article has been cited by other articles:
|
|
 |
|
  W. Liang, S. Austin, Q. Hoang, and P. H. Fishman Resistance of the Human {beta}1-Adrenergic Receptor to Agonist-mediated Down-regulation: ROLE OF THE C TERMINUS IN DETERMINING {beta}-SUBTYPE DEGRADATION J. Biol. Chem., October 10, 2003; 278(41): 39773 - 39781. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Marion-Latard, I. De Glisezinski, F. Crampes, M. Berlan, J. Galitzky, H. Suljkovicova, D. Riviere, and V. Stich A single bout of exercise induces {beta}-adrenergic desensitization in human adipose tissue Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2001; 280(1): R166 - R173. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Wang and E. M. Ross The Carboxyl-terminal Anchorage Domain of the Turkey beta(1)-Adrenergic Receptor Is Encoded by an Alternatively Spliced Exon J. Biol. Chem., March 24, 1995; 270(12): 6488 - 6495. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
