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Cardiovascular Research 2001 50(3):443-453; doi:10.1016/S0008-6363(01)00244-9
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Sympathoadrenergic mechanisms in functional regulation and development of cardiac hypertrophy and failure: findings from genetically engineered mice

Xiao-Jun Du*

Experimental Cardiology Laboratory, Baker Medical Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia

* Tel.: +61-3-9522-4333; fax: +61-3-9521-1362 xiaojun.du@baker.edu.au

Received 2 August 2000; accepted 12 February 2001

KEYWORDS Autonomic nervous system; Cardiomyopathy; Heart failure; Hypertrophy; Receptors; Signal transduction

The first 150 words of the full text of this article appear below.


   1 Introduction
 
Sympathoadrenergic signals to the heart are detected and processed by a group of membrane proteins converting external signals to alterations in intracellular properties. In recent years, our understanding of β- and {alpha}-adrenergic signaling has been significantly improved. It is beyond the scope of this review to discuss the adrenergic signaling pathways and several excellent reviews are available [1–5].

Sympathetic activation serves to maintain cardiac output by enhancing inotropy, relaxation and chronotropy. Under conditions of heart failure (HF), the sympathetic nervous system is activated chronically and enhanced cardiac sympathetic drive frequently precedes the onset of overt clinic symptoms and is one of the fundamental abnormalities in HF [6]. In the hypertrophied and failing heart, there occurs profound desensitization of β-adrenergic receptor (AR) signaling due to decreased β1AR density, uncoupling of βAR to stimulatory G-protein (Gs), diminished adenylyl cyclase (AC) activity, increased βAR kinase (βARK) activity, and elevated content . . . [Full Text of this Article]


   2 Phenotypes of mice with β- or {alpha}-adrenergic receptor disruption or overexpression
 
2.1 Disruption of βAR
2.2 Overexpression of βAR
2.2.1 β1AR
2.2.2 β2AR
2.2.3 β3AR
2.3 {alpha}AR overexpression or disruption
2.3.1 {alpha}1AAR
2.3.2 {alpha}1BAR
2.3.3 Summary

   3 Phenotype of strains overexpressing downstream components of adrenergic signaling pathways
 
3.1 AR-coupled G-proteins
3.1.1 Gs{alpha}
3.1.2 Gi
3.1.3 Gq{alpha}
3.1.4 Gh
3.2 Adenylyl cyclase
3.3 βAR kinase-1 and β-arrestins
3.3.1 βARK1
3.3.2 β-Arrestins

   4 Comparison of cardiac phenotypes of β-adrenergic signaling targeted strains
 

   5 Presynaptic factors controlling sympathetic nervous activity
 
5.1 Nerve growth factor (NGF) overexpression
5.2 Disruption of enzymes for catecholamine synthesis and metabolism
5.3 Disruption of presynaptic {alpha}2AR
5.4 Summary

   6 Gene complementation
 
6.1 Gene complementation by crossbreeding
6.2 Summary

   7 Conclusions
 

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