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1B-adrenergic receptors after pressure overload in
mouse hearts
1 Cellular Biochemistry Laboratory, 2 Experimental Cardiology Laboratory, and 3 Molecular Physiology Laboratory, Baker Medical Research Institute, Prahran 3181, Victoria, Australia; and 4 Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina 27710
Cardiac
hypertrophy and function were studied 6 wk after constriction of the
thoracic aorta (TAC) in transgenic (TG) mice expressing constitutively
active mutant 
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 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 1B-ARs is detrimental in
terms of hypertrophy and cardiac function after pressure overload and that increased 1A-AR mRNA expression is not a feature of
the hypertrophic response in this murine model.
1-adrenergic receptor; hypertrophy; heart failure; transgenic mouse; constitutively active mutant
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