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...
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Weitere Verfasser: | , , |
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Format: | Elektronisch E-Book |
Sprache: | English |
Veröffentlicht: |
Boston, MA
Springer US
2000
|
Schriftenreihe: | Progress in Experimental Cardiology
3 |
Schlagworte: | |
Online-Zugang: | UBR01 Volltext |
Zusammenfassung: | 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 |
Beschreibung: | 1 Online-Ressource (XIV, 469 p) |
ISBN: | 9781461544234 |
DOI: | 10.1007/978-1-4615-4423-4 |
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520 | |a 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 | ||
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Datensatz im Suchindex
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any_adam_object | |
author2 | Takeda, Nobuakira Nagano, Makoto Dhalla, Naranjan S. |
author2_role | edt edt edt |
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author_facet | Takeda, Nobuakira Nagano, Makoto Dhalla, Naranjan S. |
building | Verbundindex |
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dewey-full | 616.12 |
dewey-hundreds | 600 - Technology (Applied sciences) |
dewey-ones | 616 - Diseases |
dewey-raw | 616.12 |
dewey-search | 616.12 |
dewey-sort | 3616.12 |
dewey-tens | 610 - Medicine and health |
discipline | Medizin |
doi_str_mv | 10.1007/978-1-4615-4423-4 |
format | Electronic eBook |
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institution | BVB |
isbn | 9781461544234 |
language | English |
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publisher | Springer US |
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series2 | Progress in Experimental Cardiology |
spelling | The Hypertrophied Heart edited by Nobuakira Takeda, Makoto Nagano, Naranjan S. Dhalla Boston, MA Springer US 2000 1 Online-Ressource (XIV, 469 p) txt rdacontent c rdamedia cr rdacarrier Progress in Experimental Cardiology 3 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 Cardiology Herzhypertrophie (DE-588)4024652-8 gnd rswk-swf Herzhypertrophie (DE-588)4024652-8 s 1\p DE-604 Takeda, Nobuakira edt Nagano, Makoto edt Dhalla, Naranjan S. edt Erscheint auch als Druck-Ausgabe 9780792377412 Erscheint auch als Druck-Ausgabe 9781461369912 Erscheint auch als Druck-Ausgabe 9781461544241 https://doi.org/10.1007/978-1-4615-4423-4 Verlag URL des Erstveröffentlichers Volltext 1\p cgwrk 20201028 DE-101 https://d-nb.info/provenance/plan#cgwrk |
spellingShingle | The Hypertrophied Heart Cardiology Herzhypertrophie (DE-588)4024652-8 gnd |
subject_GND | (DE-588)4024652-8 |
title | The Hypertrophied Heart |
title_auth | The Hypertrophied Heart |
title_exact_search | The Hypertrophied Heart |
title_full | The Hypertrophied Heart edited by Nobuakira Takeda, Makoto Nagano, Naranjan S. Dhalla |
title_fullStr | The Hypertrophied Heart edited by Nobuakira Takeda, Makoto Nagano, Naranjan S. Dhalla |
title_full_unstemmed | The Hypertrophied Heart edited by Nobuakira Takeda, Makoto Nagano, Naranjan S. Dhalla |
title_short | The Hypertrophied Heart |
title_sort | the hypertrophied heart |
topic | Cardiology Herzhypertrophie (DE-588)4024652-8 gnd |
topic_facet | Cardiology Herzhypertrophie |
url | https://doi.org/10.1007/978-1-4615-4423-4 |
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