Abstract
Transgenic mice with intense cardiac expression of a human beta-adrenergic receptor gene were engineered and shown to display marked improvements in baseline myocardial and left ventricular function. Heart/body weight ratios and histologic appearance were not found to be significantly altered, suggesting that receptor gene expression did not induce pathologic changes. Given the substantial reduction in beta-adrenergic receptor density and resultant reduction in inotropic responsiveness observed in chronic heart failure, these findings represent a novel approach for increasing myocardial function with important clinical implications.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Atrial Natriuretic Factor / genetics
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Atrial Natriuretic Factor / metabolism
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Blotting, Northern
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Body Weight
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Female
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Gene Expression
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Gene Transfer Techniques
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Heart / anatomy & histology
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Heart Failure / therapy
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Humans
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Male
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Mice
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Mice, Transgenic
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Myocardial Contraction / physiology*
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Myocardium / metabolism*
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Myosins / genetics
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Organ Size
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Receptors, Adrenergic, beta-2 / genetics*
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Receptors, Adrenergic, beta-2 / physiology
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Ventricular Function, Left / genetics*
Substances
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Receptors, Adrenergic, beta-2
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Atrial Natriuretic Factor
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Myosins