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The Hypertrophied Heart

Part of the book series: Progress in Experimental Cardiology (PREC, volume 3)

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Table of contents (37 chapters)

  1. Front Matter

    Pages i-xiv
  2. Mechanisms of Cardiac Hypertrophy

    1. Front Matter

      Pages 1-1
    2. Regulation of Ribosomal DNA Transcription During Cardiomyocyte Hypertrophy

      • Toru Arino, Ross D. Hannan, Kiyofumi Suzuki, Lawrence I. Rothblum
      Pages 31-40
    3. Mitochondrial Gene Expression in Hypertrophic Cardiac Muscles in Rats

      • Taro Murakami, Yoshiharu Shimomura, Li Zhihao, Kazuyuki Shimizu, Satoru Sugiyama
      Pages 41-49
    4. SERCA2 and ANF Promoter-Activity Studies in Hypertrophic Cardiomyocytes Using Liposome-, Gene Gun-, and Adenovirus-Mediated Gene Transfer

      • Karin Eizema, Han A. A. Van Heugten, Karel Bezstarosti, Marga C. Van Setten, Sonja Schneider-Rasp, Wolfgang C. Poller et al.
      Pages 51-66
    5. Ca2+ Transients, Contractility, and Inotropic Responses in Rabbit Volume-Overloaded Cardiomyocytes

      • Kiyoharu Sakurai, Hiromi Sugawara, Tomoo Watanabe, Shigekazu Nakada, Hiroyuki Atsumi, Hitonobu Tomoike et al.
      Pages 67-81
    6. Responsiveness of Contractile Elements to Muscle Length Change in Hyperthyroid Ferret Myocardium

      • Tetsuya Ishikawa, Hidetoshi Kajiwara, Seibu Mochizuki, Satoshi Kurihara
      Pages 83-90
    7. Possible Roles of the Tenascin Family During Heart Development and Myocardial Tissue Remodeling

      • Kyoko Imanaka-Yoshida, Kazuto Yokoyama, Teruyo Sakakura
      Pages 123-129
    8. Cardiac Cell-ECM Interactions: A Possible Site for Mechanical Signaling

      • Shalini Kanekar, Wayne Carver, Thomas K. Borg, Joel Atance, Louis Terracio
      Pages 131-141
    9. Integrin-Dependent and -Independent Signaling During Pressure-Overload Cardiac Hypertrophy

      • Martin Laser, Toshio Nagai, Vijaykumar S. Kasi, Catalin F. Baicu, Christopher D. Willey, Charlene M. Kerr et al.
      Pages 143-164
    10. Role of G Proteins in Hypertension and Hypertrophy

      • Madhu B. Anand-Srivastava, Francesco Di Fusco
      Pages 165-178
    11. Three-Dimensional Nuclear Size and DNA Content in Hypertensive Heart Disease

      • Atsushi Takeda, Yuusaku Hayashi, Chihiro Shikata, Yasuyuki Tanaka, Nobuakira Takeda
      Pages 179-186
    12. Age-Related Anisotropic Changes in Cardiocyte Connections in Spontaneously Hypertensive Rats

      • Makoto Okabe, Keishiro Kawamura, Fumio Terasaki, Tetsuya Hayashi, Yumiko Kanzaki, Haruhiro Toko
      Pages 187-196
    13. Adaptation of the Poikilothermic Heart to Catecholamine-Induced Overload

      • Bohuslav Ostadal, Vaclav Pelouch, Arnost Bass, Pavel Pucelik, Olga Novakova
      Pages 217-226

About this book

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.

Editors and Affiliations

  • Department of Internal Medicine, Aoto Hospital, Jikei University School of Medicine, Tokyo, Japan

    Nobuakira Takeda

  • Jikei University School of Medicine, Tokyo, Japan

    Makoto Nagano

  • Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Canada

    Naranjan S. Dhalla

Bibliographic Information

  • Book Title: The Hypertrophied Heart

  • Editors: Nobuakira Takeda, Makoto Nagano, Naranjan S. Dhalla

  • Series Title: Progress in Experimental Cardiology

  • DOI: https://doi.org/10.1007/978-1-4615-4423-4

  • Publisher: Springer New York, NY

  • eBook Packages: Springer Book Archive

  • Copyright Information: Springer Science+Business Media New York 2000

  • Hardcover ISBN: 978-0-7923-7741-2Published: 30 September 2000

  • Softcover ISBN: 978-1-4613-6991-2Published: 13 October 2012

  • eBook ISBN: 978-1-4615-4423-4Published: 06 December 2012

  • Series ISSN: 1389-1774

  • Edition Number: 1

  • Number of Pages: XIV, 469

  • Topics: Cardiology

Buy it now

Buying options

eBook USD 129.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book USD 169.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book USD 169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Other ways to access