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 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.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000468:Alkalies / Q000494:pharmacology; D001692:Biological Transport; D002301:Cardiac Glycosides / Q000494:pharmacology; D002395:Catecholamines / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D006321:Heart / Q000502:physiology*; D008274:Magnesium / Q000494:pharmacology; D009119:Muscle Contraction; D009124:Muscle Proteins / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D000468:Alkalies; D002301:Cardiac Glycosides; D002395:Catecholamines; D009124:Muscle Proteins; D012964:Sodium; D000251:Adenosine Triphosphatases; D008274:Magnesium; D011188:Potassium