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Mechanical Stress, Local Renin-Angiotensin System and Cardiac Hypertrophy: An Overview

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Part of the book series: Progress in Experimental Cardiology ((PREC,volume 2))

Summary

Hypertrophy is a fundamental adaptive process employed by postmitotic cardiac and skeletal muscles in response to mechanical load. External load also plays a critical role in determining muscle mass and its phenotype in cardiac myocytes. Interestingly, cardiac myocytes have the intrinsic ability to sense mechanical stretch and convert it into intracellular growth signals, which finally culminate in hypertrophic growth. Mechanical stretch of cardiac myocytes in vitro causes activation of multiple messenger systems, upregulation of many immediate early genes (e.g., c-fos, c-myc, c-jun, etc.), and re-expression of fetal-type genes (e.g., atrial natriuretic factor, skeletal a-actin, β-myosin heavy chain), reminiscent of cardiac hypertrophy in vivo. Stretch of neonatal rat cardiac myocytes stimulates a rapid secretion of angiotensin (Ang) II and an upregulation of all major components of cardiac renin-angiotensin system (RAS) genes. Ang II, along with other (secreted) growth factors, mediates many, if not all, stretch-induced hypertrophic responses. In this review, the relationship between mechanical loading, cardiac RAS, and cardiac hypertrophy is discussed. In addition, various cell signaling mechanisms initiated by mechanical stress on cardiac myocytes are briefly summarized.

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Malhotra, R., Izumo, S. (1998). Mechanical Stress, Local Renin-Angiotensin System and Cardiac Hypertrophy: An Overview. In: Dhalla, N.S., Zahradka, P., Dixon, I.M.C., Beamish, R.E. (eds) Angiotensin II Receptor Blockade Physiological and Clinical Implications. Progress in Experimental Cardiology, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5743-2_21

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