Adverse effects of constitutively active alpha(1B)-adrenergic receptors after pressure overload in mouse hearts.


Journal Article

Cardiac hypertrophy and function were studied 6 wk after constriction of the thoracic aorta (TAC) in transgenic (TG) mice expressing constitutively active mutant alpha(1B)-adrenergic receptors (ARs) in the heart. Hearts from sham-operated TG animals and nontransgenic littermates (WT) were similar in size, but hearts from TAC/TG mice were larger than those from TAC/WT mice, and atrial natriuretic peptide mRNA expression was also higher. Lung weight was markedly increased in TAC/TG animals, and the incidence of left atrial thrombus formation was significantly higher. Ventricular contractility in anesthetized animals, although it was increased in TAC/WT hearts, was unchanged in TAC/TG hearts, implying cardiac decompensation and progression to failure in TG mice. There was no increase in alpha(1A)-AR mRNA expression in TAC/WT hearts, and expression was significantly reduced in TAC/TG hearts. These findings show that cardiac expression of constitutively actively mutant alpha(1B)-ARs is detrimental in terms of hypertrophy and cardiac function after pressure overload and that increased alpha(1A)-AR mRNA expression is not a feature of the hypertrophic response in this murine model.

Full Text

Duke Authors

Cited Authors

  • Wang, BH; Du, XJ; Autelitano, DJ; Milano, CA; Woodcock, EA

Published Date

  • September 2000

Published In

Volume / Issue

  • 279 / 3

Start / End Page

  • H1079 - H1086

PubMed ID

  • 10993770

Pubmed Central ID

  • 10993770

International Standard Serial Number (ISSN)

  • 0363-6135

Digital Object Identifier (DOI)

  • 10.1152/ajpheart.2000.279.3.H1079


  • eng

Conference Location

  • United States