Left ventricular hypertrophy is considered to be an independent risk factor giving rise to ischemia, arrhythmias, and left ventricular dysfunction. Slow movement of intracellular calcium contributes to the impaired contraction and relaxation function of hypertrophied myocardium. Myofibril content may also be shifted to fetal-type isoforms with decreased contraction and relaxation properties in left ventricular hypertrophy. Myocyte hypertrophy and interstitial fibrosis are regulated independently by mechanical and neurohumoral mechanisms. In severely hypertrophied myocardium, capillary density is reduced, the diffusion distance for oxygen, nutrients, and metabolites is increased, and the ratio of energy-production sites to energy-consumption sites is decreased. The metabolic state of severely hypertrophied myocardium is anaerobic, as indicated by the shift of lactate dehydrogenase marker enzymes. Therefore, the hypertrophied myocardium is more vulnerable to ischemie events. As a compensatory response to severe cardiac hypertrophy and congestive heart failure, the ADP/ATP carrier is activated and atrial natriuretic peptide is released to increase high-energy phosphate production and reduce cardiac energy consumption by vasodilation and sodium and fluid elimination. However, in severely hypertrophied and failing myocardium, vasoconstrictor and sodium- and fluid-retaining factors, such as the renin-angiotensin system, aldosterone, and sympathetic nerve activity, play an overwhelming role. Angiotensin-converting enzyme inhibitors (ACEIs) are able to prevent cardiac hypertrophy and improve cardiac function and metabolism. Under experimental conditions, these beneficial effects can be ascribed mainly to bradykinin potentiation, although a contribution of the ACEI-induced angiotensin II reduction cannot be excluded.
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January 01 1996
Substrate Metabolism, Hormone Interaction, and Angiotensin-Converting Enzyme Inhibitors in Left Ventricular Hypertrophy
Yi-chun Zhu;
Yi-chun Zhu
Department of Pharmacology, Christian Albrechts University of Kiel
Kiel, Germany
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Yi-zhun Zhu;
Yi-zhun Zhu
Department of Pharmacology, Christian Albrechts University of Kiel
Kiel, Germany
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Heidi Spitznagel;
Heidi Spitznagel
Department of Pharmacology, Christian Albrechts University of Kiel
Kiel, Germany
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Peter Gohlke;
Peter Gohlke
Department of Pharmacology, Christian Albrechts University of Kiel
Kiel, Germany
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Thomas Unger
Thomas Unger
Department of Pharmacology, Christian Albrechts University of Kiel
Kiel, Germany
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Address correspondence and reprint requests to Dr. Thomas Unger, Department of Pharmacology, Christian Albrechts University of Kiel, Hospitalstrasse 4, 24105 Kiel, Germany
Citation
Yi-chun Zhu, Yi-zhun Zhu, Heidi Spitznagel, Peter Gohlke, Thomas Unger; Substrate Metabolism, Hormone Interaction, and Angiotensin-Converting Enzyme Inhibitors in Left Ventricular Hypertrophy. Diabetes 1 January 1996; 45 (Supplement_1): S59–S65. https://doi.org/10.2337/diab.45.1.S59
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