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Cardiac Hypertrophy and the Renin-Angiotensin System

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Cardiac-Vascular Remodeling and Functional Interaction

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Summary

In hearts with myocardial damage secondary to myocardial infarction, chronic ischemia, inflammation, or pressure or volume overload, there is a complex sequence of compensatory events that ultimately result in an adversely remodeled myocardium and a dilated, thin-walled, spherical ventricle. For a period of time, a preclinical heart failure state may exist in which there is ventricular dysfunction caused by myocardial damage but no clinical evidence of cardiac insufficiency, circulatory congestion, or edema. However, in an attempt to maintain this state, there are ongoing myocardial adaptations resulting in a continual state of remodeling with progressive ventricular dilatation mediated by changes in myocyte morphology, intracellular calcium regulation, and extracellular matrix production. Although a number of growth-promoting factors have been implicated in cardiac hypertrophy and remodeling, angiotensin II (ANG II) is assumed to play a major role in this process because it is a potent growth factor for myocytes and fibroblasts in the heart [1,2]. It has been postulated that the cardiac renin-angiotensin system (RAS) is activated during compensated heart failure and that the continued presence of ANG II could have important local pathological functions in the transition to heart failure (Fig. 1). Alternatively, the heart is a target organ for ANG II, which produces a positive inotropic and chrono tropic effect on myocytes [4–6], stimulates the release of norepinephrine from cardiac sympathetic nerves [7,8], and acts as a growth factor for myocytes [1,2]. Thus, the failing heart may be dependent on local ANG II production to provide inotropic support and to promote myocyte hypertrophy to minimize wall stress. However, the identification of alternative ANG II-forming mechanisms in the heart and the role of angiotensin-converting enzyme (ACE) on bradykinin degradation have raised questions regarding the mechanism of ANG II production in the heart and the role of ANG II per se in cardiac hypertrophy and remodeling. This chapter reviews these issues and the results of animal models investigating the cardiac renin-angiotensin system in cardiac hypertrophy caused by pressure and volume overload.

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Authors and Affiliations

  1. Birmingham Veteran Affairs Medical Center, University of Alabama at Birmingham, USA

    Louis J. Dell’Italia

  2. Department of Medicine, Division of Cardiovascular Disease, University Station, Birmingham, 35294, AL, USA

    Louis J. Dell’Italia

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Editors and Affiliations

  1. First Department of Internal Medicine, Fukushima Medical College, Hikariga-oka 1, 960-12, Fukushima, Japan

    Yukio Maruyama M.D., Ph.D. (Professor and Chairman) (Professor and Chairman)

  2. First Department of Medicine, Osaka University School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565, Japan

    Masatsugu Hori M.D., Ph.D. (Chief) (Chief)

  3. College of Veterinary Medicine, Auburn University, 106 Greene Hall, 36849-5517, Auburn, AL, USA

    Joseph S. Janicki Ph.D. (Professor, Associate Dean of Research and Graduate Studies) (Professor, Associate Dean of Research and Graduate Studies)

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Dell’Italia, L.J. (1997). Cardiac Hypertrophy and the Renin-Angiotensin System. In: Maruyama, Y., Hori, M., Janicki, J.S. (eds) Cardiac-Vascular Remodeling and Functional Interaction. Springer, Tokyo. https://doi.org/10.1007/978-4-431-67041-4_5

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  • DOI: https://doi.org/10.1007/978-4-431-67041-4_5

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