The Hypertrophied Heart

Whenever the heart is challenged with an increased work load for a prolonged period, it responds by increasing its muscle mass--a phenomenon known as cardiac hypertrophy. Although cardiac hypertrophy is commonly seen under physiological conditions such as development and exercise, a wide variety of pathological situa tions such as hypertension (pressure overload), valvular defects (volume overload), myocardial infarction (muscle loss), and cardiomyopathy (muscle disease) are also known to result in cardiac hypertrophy. Various hormones such as catecholamines, thyroid hormones, angiotensin II, endothelin, and growth factors have also been shown to induce cardiac hypertrophy. Although the exact mechanisms underlying or pathological forrns of cardiac hypertrophy are poorly under the physiological stood, an increase in the intraventricular pressure is believed to represent the major stimulus for the development of cardiac hypertrophy. In this regard, stretching of the cardiac muscle has been shown to induce the hypertrophic response, but the role of metabolic influences in this process cannot be ruled out. Furthermore, different hormones and other interventions in the absence of stretch have been observed to stimulate protein synthesis in both isolated cardiomyocyte and vascular myocyte preparations. Nonetheless, it is becoming dear that receptor as well as phospholipid linked signal transduction pathways are activated in some specific manner depend ing upon the initial hypertrophic stimulus, and these then result in an increase in the size and mass of cardiomyocytes.

List of contents

A. Mechanisms of Cardiac Hypertrophy.- 1. Signal Transduction in the Adapted Heart: Implication of Protein Kinase C-Dependent and -Independent Pathways.- 2. Glucose-6-phosphate Dehydrogenase: A Marker of Cardiac Hypertrophy.- 3. Regulation of ribosomal DNA Transcription During Cardiomyocyte Hypertrophy.- 4. Mitochondrial Gene Expression in Hypertrophic Cardiac Muscles in Rats.- 5. SERCA2 and ANF Promoter-Activity Studies in Hypertrophic Cardiomyocytes using Liposome-, Gene Gun- and Adenovirus-Mediated Gene Transfer.- 6. Ca2+ Transients, Contractility, and Inotropic Responses in RabbitVolume-Overloaded Cardiomyocytes.- 7. Responsiveness of Contractile Elements to Muscle Length Change in Hyperthyroid Ferret Myocardium.- 8. Contraction-Dependent Hyprtrophy of Neonatal Rat Ventricular Myocytes: Potential Role for Focal Adhesion Kinase.- 9. Molecular Mechanism of Mechanic Stress-Induced Cardiac Hypertrophy.- 10. Possible Roles of the Tenascin Family During Heart Deverlopment and Myocardiac Tissue Remodeling.- 11. Cardiac Cell-ECM Interactions: A Possible Site for Mechanical Signaling.- 12. Integrin-Dependent and -Independent Signaling During Pressure-Overload Cardiac Hypertrophy.- 13. Role of G Proteins in Hypertension and Hypertrophy.- 14. Three-Dimensional Nuclear Size and DNA Content in Hypertensive Heart Disease.- 15. Age-Related Anisotropic Changes in Cardiocyte Connections in Spontaneously Hypertensive Rats.- 16. Stimulation of Mitogen-Activated Protein Kinases ERK-1 and ERK-2 by H2O2 in Vascular Smooth Muscle cells.- 17. Effects of Renin-Angiotensin System Inhibition on Cardiac Hypertrophy and Fibrosis in Spontaneously Hypertensive Rats.- 18. Adaptation of the Poikilothermic Heart to Catecholamine-Induced Overload.- 19. Angiogenesis and Fibrosis During RightVentricular Hypertrophy in Human Tetralogy of Fallot.- 20. Molecular Mechanisms of Phenotypic Modulation of Vascular Smooth Muscle Cells.- B. Cardiac Failure in the Hypertrophied Heart.- 21. Protein Kinase C Activation in Cardiac Hypertrophy and Failure.- 22. Angiotensin II and Connective Tissue Homeostasis.- 23. Beneficial Effects of Angiotensin Blockade in Heart Failure due to Myocardial Infarction.- 24. Activated TGF? Signaling in the Heart After Myocardial Infarction.- 25. gp130-Dependent Signaling Pathways: Recent Advances and Implications for Cardiovascular Disease.- 26. Molecular Genetic Aspects of Hypertrophic Cadiomyopathy in the Oriental.- 27. Hepatitis C Virus Infection in Hypertrophic or Dilated Cardiomyopathy.- 28. Enhancement of Early Diastolic Filling Provoded by Dobutamine Infusion in Dilated Cardiomyopathy.- 29. DNA Fragmentation is a Possible Mechanism for Heart Failure in Cardiomyopathy.- 30. The Difference in Phosphorylation of Desmin and Myosin Light Chain 2 in the Bio 14.6 Cardiomyopathic Heart.- 31. Cardiac Remodeling in Cardiomyopathic Hamster Hearts.- 32. Human Myocardial Na,K-ATPase in Remodeling.- 33. Nitric Oxide Synthase Gene Transfer Inhibits Protein Synthesis of Rat Cardiac Mycocytes.- 34. Human Heart Failure: A Mechanistic Assessment of Altered Ventricular Function.- 35. The Structural Correlate of Reduced Cardiac Function in Failing Human Hearts.- 36. Diastilic Dysfunction and Diastolic Heart Failure.- 37. Effect of Melatonin on Cardiac Function and Metabolism in the Ischemic Working Rat Heart.

Summary

Whenever the heart is challenged with an increased work load for a prolonged period, it responds by increasing its muscle mass--a phenomenon known as cardiac hypertrophy. Although cardiac hypertrophy is commonly seen under physiological conditions such as development and exercise, a wide variety of pathological situa­ tions such as hypertension (pressure overload), valvular defects (volume overload), myocardial infarction (muscle loss), and cardiomyopathy (muscle disease) are also known to result in cardiac hypertrophy. Various hormones such as catecholamines, thyroid hormones, angiotensin II, endothelin, and growth factors have also been shown to induce cardiac hypertrophy. Although the exact mechanisms underlying or pathological forrns of cardiac hypertrophy are poorly under­ the physiological stood, an increase in the intraventricular pressure is believed to represent the major stimulus for the development of cardiac hypertrophy. In this regard, stretching of the cardiac muscle has been shown to induce the hypertrophic response, but the role of metabolic influences in this process cannot be ruled out. Furthermore, different hormones and other interventions in the absence of stretch have been observed to stimulate protein synthesis in both isolated cardiomyocyte and vascular myocyte preparations. Nonetheless, it is becoming dear that receptor as well as phospholipid­ linked signal transduction pathways are activated in some specific manner depend­ ing upon the initial hypertrophic stimulus, and these then result in an increase in the size and mass of cardiomyocytes.

Product details

• Assisted by: Naranjan S. Dhalla (Editor), Makot Nagano (Editor), Makoto Nagano (Editor), Naranjan S Dhalla (Editor), Nobuakira Takeda (Editor)
• Publisher: Springer, Berlin
• Languages: English
• Product format: Paperback / Softback
• Released: 13.03.2013
• EAN: 9781461369912
• ISBN: 978-1-4613-6991-2
• No. of pages: 469
• Dimensions: 155 mm x 26 mm x 235 mm
• Weight: 727 g
• Illustrations: XIV, 469 p.
• Series: Progress in Experimental Cardiology; Progress in Experimental Cardiology
• Subject: Natural sciences, medicine, IT, technology > Medicine > Non-clinical medicine