Myocardial beta-adrenergic receptor signaling in vivo: insights from transgenic mice.


Journal Article (Review)

Heart failure is a problem of increasing importance in cardiovascular medicine. An important characteristic of heart failure is reduced agonist-stimulated adenylyl cyclase activity (receptor desensitization) due to both diminished receptor number (receptor downregulation) and impaired receptor function (receptor uncoupling). These changes in the section-adrenergic receptor (section-AR) system may in part account for some of the abnormalities of contractile function in this disease. Myocardial contraction is closely regulated by G protein coupled beta-adrenergic receptors through the action of the second messenger cAMP. The beta-adrenergic receptors themselves are regulated by a set of specific kinases, termed the G-protein-coupled receptor kinases. The study of this complex system in vivo has recently been advanced by the development of transgenic and gene targeted ("knockout") mouse models. Combining transgenic technology with sophisticated physiological measurements of cardiac hemodynamics is an extremely powerful strategy to study the regulation of myocardial contractility in the normal and failing heart.

Full Text

Duke Authors

Cited Authors

  • Rockman, HA; Koch, WJ; Milano, CA; Lefkowitz, RJ

Published Date

  • September 1996

Published In

Volume / Issue

  • 74 / 9

Start / End Page

  • 489 - 495

PubMed ID

  • 8892053

Pubmed Central ID

  • 8892053

International Standard Serial Number (ISSN)

  • 0946-2716

Digital Object Identifier (DOI)

  • 10.1007/BF00204974


  • eng

Conference Location

  • Germany