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Research Article Free access | 10.1172/JCI119086

Elevated blood pressure and enhanced myocardial contractility in mice with severe IGF-1 deficiency.

G Lembo, H A Rockman, J J Hunter, H Steinmetz, W J Koch, L Ma, M P Prinz, J Ross Jr, K R Chien, and L Powell-Braxton

Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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Published December 1, 1996 - More info

Published in Volume 98, Issue 11 on December 1, 1996
J Clin Invest. 1996;98(11):2648–2655. https://doi.org/10.1172/JCI119086.
© 1996 The American Society for Clinical Investigation
Published December 1, 1996 - Version history
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Abstract

To circumvent the embryonic lethality of a complete deficiency in insulin-like growth factor 1 (IGF-1), we generated mice homozygous for a site-specific insertional event that created a mutant IGF-1 allele (igf1m). These mice have IGF-1 levels 30% of wild type yet survive to adulthood, thereby allowing physiological analysis of the phenotype. Miniaturized catheterization technology revealed elevated conscious blood pressure in IGF-1(m/m) mice, and measurements of left ventricular contractility were increased. Adenylyl cyclase activity was enhanced in IGF-1(m/m) hearts, without an increase in beta-adrenergic receptor density, suggesting that crosstalk between IGF-1 and beta-adrenergic signaling pathways may mediate the increased contractility. The hypertrophic response of the left ventricular myocardium in response to aortic constriction, however, was preserved in IGF-1(m/m) mice. We conclude that chronic alterations in IGF-1 levels can selectively modulate blood pressure and left ventricular function, while not affecting adaptive myocardial hypertrophy in vivo.

Version history
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