Regulation of Cardiac Muscle Contractility
The heart's physiological performance, unlike that of skeletal muscle, is regulated primarily by variations in the contractile force developed by the individual myocardial fibers. In an attempt to identify the basis for the characteristic properties of myocardial contraction, the individual ca...
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| Format: | Online |
| Language: | English |
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The Rockefeller University Press
1967
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2225748/ |
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pubmed-2225748 |
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pubmed-22257482008-04-23 Regulation of Cardiac Muscle Contractility Katz, Arnold M. Comparative Aspects of Muscular Contraction The heart's physiological performance, unlike that of skeletal muscle, is regulated primarily by variations in the contractile force developed by the individual myocardial fibers. In an attempt to identify the basis for the characteristic properties of myocardial contraction, the individual cardiac contractile proteins and their behavior in contractile models in vitro have been examined. The low shortening velocity of heart muscle appears to reflect the weak ATPase activity of cardiac myosin, but this enzymatic activity probably does not determine active state intensity. Quantification of the effects of Ca++ upon cardiac actomyosin supports the view that myocardial contractility can be modified by changes in the amount of calcium released during excitation-contraction coupling. Exchange of intracellular K+ with Na+ derived from the extracellular space also could enhance myocardial contractility directly, as highly purified cardiac actomyosin is stimulated when K+ is replaced by an equimolar amount of Na+. On the other hand, cardiac glycosides and catecholamines, agents which greatly increase the contractility of the intact heart, were found to be without significant actions upon highly purified reconstituted cardiac actomyosin. The Rockefeller University Press 1967-07-01 /pmc/articles/PMC2225748/ /pubmed/4227923 Text en Copyright © 1967 by The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Katz, Arnold M. |
| spellingShingle |
Katz, Arnold M. Regulation of Cardiac Muscle Contractility |
| author_facet |
Katz, Arnold M. |
| author_sort |
Katz, Arnold M. |
| title |
Regulation of Cardiac Muscle Contractility |
| title_short |
Regulation of Cardiac Muscle Contractility |
| title_full |
Regulation of Cardiac Muscle Contractility |
| title_fullStr |
Regulation of Cardiac Muscle Contractility |
| title_full_unstemmed |
Regulation of Cardiac Muscle Contractility |
| title_sort |
regulation of cardiac muscle contractility |
| description |
The heart's physiological performance, unlike that of skeletal muscle, is regulated primarily by variations in the contractile force developed by the individual myocardial fibers. In an attempt to identify the basis for the characteristic properties of myocardial contraction, the individual cardiac contractile proteins and their behavior in contractile models in vitro have been examined. The low shortening velocity of heart muscle appears to reflect the weak ATPase activity of cardiac myosin, but this enzymatic activity probably does not determine active state intensity. Quantification of the effects of Ca++ upon cardiac actomyosin supports the view that myocardial contractility can be modified by changes in the amount of calcium released during excitation-contraction coupling. Exchange of intracellular K+ with Na+ derived from the extracellular space also could enhance myocardial contractility directly, as highly purified cardiac actomyosin is stimulated when K+ is replaced by an equimolar amount of Na+. On the other hand, cardiac glycosides and catecholamines, agents which greatly increase the contractility of the intact heart, were found to be without significant actions upon highly purified reconstituted cardiac actomyosin. |
| publisher |
The Rockefeller University Press |
| publishDate |
1967 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2225748/ |
| _version_ |
1611436779340038144 |