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Research Article Free access | 10.1172/JCI114576

Hypertensive cardiomyopathy. Myocyte nuclei hyperplasia in the mammalian rat heart.

P Anversa, T Palackal, E H Sonnenblick, G Olivetti, and J M Capasso

Department of Pathology, New York Medical College, Valhalla 10595.

Find articles by Anversa, P. in: JCI | PubMed | Google Scholar

Department of Pathology, New York Medical College, Valhalla 10595.

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Department of Pathology, New York Medical College, Valhalla 10595.

Find articles by Sonnenblick, E. in: JCI | PubMed | Google Scholar

Department of Pathology, New York Medical College, Valhalla 10595.

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Department of Pathology, New York Medical College, Valhalla 10595.

Find articles by Capasso, J. in: JCI | PubMed | Google Scholar

Published April 1, 1990 - More info

Published in Volume 85, Issue 4 on April 1, 1990
J Clin Invest. 1990;85(4):994–997. https://doi.org/10.1172/JCI114576.
© 1990 The American Society for Clinical Investigation
Published April 1, 1990 - Version history
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Abstract

To determine whether long-term hypertension leads to hyperplasia of myocyte nuclei in the heart, a phenomenon suspected to occur in humans, renal hypertension was produced in rats and the animals were killed 8 mo later. Arterial blood pressure remained elevated for approximately 5 mo, but decreased progressively in the last 3 mo so that at 8 mo this parameter was practically identical to that found in controls. Moreover, left ventricular end diastolic pressure was markedly increased in experimental animals in association with a substantial decrease in left ventricular dP/dt. The alteration of these physiological measurements was indicative of severe ventricular dysfunction. Quantitative analysis of the transmural distribution of myocyte nuclei in the left ventricle showed 36 and 23% increases in myocyte nuclei concentration in the epimyocardium and endomyocardium, respectively. These changes in nuclei were accompanied by 25 and 16% reductions in myocyte cell volume per nucleus in the outer and inner layers of the wall. In conclusion, long-term hypertension leads to impairment of ventricular function and proliferation of nuclei in myocytes.

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