Effects of calcium on the sarcomere length-tension relation in rat cardiac muscle. Implications for the Frank-Starling mechanism.

Gordon, A. M.; Pollack, G H

doi:10.1161/01.res.47.4.610

Cited by 43 publications

(26 citation statements)

References 31 publications

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“…The role of changing contraction duration, induced deactivation, and increased activation in the immediate enhancement of myocardial performance due to lengthening have recently been discussed (Jewell, 1977;Gordon and Pollack, 1980), and it is not clear that the present experiments shed further light on this subject.…”

Section: Discussionmentioning

confidence: 85%

“…Activation factors which most likely depend on muscle length have been recently considered (Jewell, 1977;Gordon and Pollack, 1980) as including: (1) changing of contraction duration, (2) decreased deactivation, and (3) increased activation. As the slow increase of pressure occurred at a constant ventricular volume, the most straightforward conclusion is that slow changes take place when muscle fibers are at near-constant length.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the Frank-Starling mechanism and contractility generally are considered as quite separate mechanisms regulating ventricular performance. Recent studies undertaken in isolated cardiac muscle preparations suggest that changes in the activation process occur with changes in muscle length (Allen et al, 1974;Fabiato and Fabiato, 1975;Lakatta and Jewell, 1977;Lakatta and Henderson, 1977;Huntsman and Stewart, 1977;Ter Keurs et al, 1980;Gordon and Pollack, 1980;Allen and Kurihara, 1982). As a consequence, a new concept has emerged: that muscle length influences inotropic state, and, therefore, a change of muscle length must be regarded as an inotropic intervention.…”

Section: Length Dependence Of Activation Studied In the Isovolumic Blmentioning

confidence: 99%

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Length dependence of activation studied in the isovolumic blood-perfused dog heart.

Tucci¹,

Bregagnollo²,

Spadaro³

et al. 1984

Circulation Research

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SUMMARY. In studies utilizing the isolated isovolumic blood-perfused canine heart, left ventricular pressure was measured following a sudden expansion of ventricular volume. An increase in performance occurred in two phases: first, there was an instantaneous rise of developed pressure simultaneous with ventricular distension; in the second phase, developed pressure continued to increase for several minutes until a final steady state was reached. The immediate increase in developed pressure occurred with a prolongation of the time-to-peak pressure, and there was no further change of time-to-peak pressure during the time-dependent increase of developed pressure. In another series of experiments, systolic pressure was elevated without changing resting volume, and mechanical performance changed in a different manner: after an increase in systolic load, there was a modest and transient decrease of developed pressure; thereafter, ventricular pressure recovered only to original values. The influence of different degrees of ventricular expansion, calcium, and verapamil were studied. Under higher ventricular dilations the immediate as well as the slow increase of contraction were heightened and the time to reach half of the slow increase was shortened. When ventricular dilation was induced during an infusion of calcium chloride, higher values for the immediate pressure increase were observed, whereas the timedependent increase and the time to reach half of the slow increase did not change in comparison with control studies. Verapamil decreased the immediate and the time-dependent enhancement of contraction. The time-dependent increase in developed pressure occurs more slowly with verapamil. These findings in the intact heart are in accord with the hypothesis that myocardial stretch is followed by an increase in intracellular calcium stores, and with the concept that the Frank-Starling mechanism involves an activation of the contractile state. (Circ Res 55: 59-66, 1984)

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Length Dependence Of Activation Studied In the Isovolumic Blmentioning

confidence: 99%

See 1 more Smart Citation

Length dependence of activation studied in the isovolumic blood-perfused dog heart.

Tucci¹,

Bregagnollo²,

Spadaro³

et al. 1984

Circulation Research

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“…The molecular basis of this intrinsic system is not known. It has been speculated to reflect better alignment of the myofibrillar arrays (Sonnenblick et al 1973) or regulation of intracellular calcium (Ca 2+ ) (Gordon and Pollack 1980;Van Henningen et al 1982;Gillebert et al 1989). Even the embryonic heart manifests a Frank-Starling response well before innervation (Benson et al 1989).…”

mentioning

confidence: 99%

VEGF–PLCγ1 pathway controls cardiac contractility in the embryonic heart

Rottbauer¹,

Just²,

Wessels³

et al. 2005

Genes Dev.

125

104

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The strength of the heart beat can accommodate in seconds to changes in blood pressure or flow. The mechanism for such homeostatic adaptation is unknown. We sought the cause of poor contractility in the heart of the embryonic zebrafish with the mutation dead beat. We find through cloning that this is due to a mutation in the phospholipase C ␥1 (plc␥1) gene. In mutant embryos, contractile function can be restored by PLC␥1 expression directed selectively to cardiac myocytes. In other situations, PLC␥1 is known to transduce the signal from vascular endothelial growth factor (VEGF), and we show here that abrogation of VEGF also interferes with cardiac contractility. Somewhat unexpectedly, FLT-1 is the responsible VEGF receptor. We show that the same system functions in the rat. Blockage of VEGF-PLC␥1 signaling decreases calcium transients in rat ventricular cardiomyocytes, whereas VEGF imposes a positive inotropic effect on cardiomyocytes by increasing calcium transients. Thus, the muscle of the heart uses the VEGF-PLC␥1 cascade to control the strength of the heart beat. We speculate that this paracrine system may contribute to normal and pathological regulation of cardiac contractility.[Keywords: VEGF; PLC␥1; contractility; heart; zebrafish] Supplemental material is available at http://www.genesdev.org.

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“…GORDON and POLLACK [19] measured the effect of calcium on the sarcomere length-tension curve in thin trabeculae from rat right ventricle and confirmed that the height of the curve was progressively depressed as extracellular calcium levels were reduced from 2.5 to 0.3 mM (similarly to curves 5 to 3 in Fig. 3).…”

Section: Force-velocity Relation Of Tetanized Cardiac Musclementioning

confidence: 67%

Force-velocity relation and contractility in striated muscles.

Mashima

1984

Jpn.J.Physiol

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This review deals with the contractility of striated muscles as made evident in the force and the shortening velocities in various contractions. The contractility, that is, the capability of contraction, can be expressed using two parameters. One is the maximum tension during isometric contraction and the other, the maximum shortening velocity during isotonic contraction under zero load.Shortening velocity is a function of load, which is equal to the muscle tension during isotonic contraction, and the maximum tension, Tm, can be obtained from the full isometric tetanic contraction at the optimal muscle length, Lm. Therefore, the most important way of ascertaining contractility is to determine the relation between tension and velocity, i.e., the force-velocity relation, at the initial length of Lm. Figure 1 is a three-dimensional illustration of contractility, in which force-velocity curves (a, b, and c) are depicted on the T -v plane and a tension-length curve (dl, descending limb; d2, ascending limb) is on the T -L plane. The curve a is a typical force-velocity curve obtained at Lm where the isometric tension, Tm, is true maximum tension, and the shortening velocity under zero load, vm, is true maximum velocity. In the curve b the isometric tension, Tb, is smaller than Tm, because the muscle is not fully but partially activated. In the curve c, the muscle is fully activated, but the isometric tension, To, is also smaller than Tm, because the initial length, Lo, is different from Lm. Whether the maximum shortening velocities obtained under various conditions, such as represented by curves b and c, are equal or not and the nature of the theoretical explanation of the force-velocity curve from the viewpoint of the recently constructed crossbridge model are the main concerns of this review. A. FORCE-VELOCITY RELATION OF SKELETAL MUSCLES Hill's characteristic equationThe force-velocity relation of skeletal muscle at Lm was described by HILL [22] for the isotonic shortening of the frog sartorius muscle in terms of a simple hyperbolic "characteristic equation," (T+a)(v+b)=b(Tm+a)=const.,where T is the load equal to the tension during isotonic shortening, v is the shorten-1

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Effects of calcium on the sarcomere length-tension relation in rat cardiac muscle. Implications for the Frank-Starling mechanism.

Cited by 43 publications

References 31 publications

Length dependence of activation studied in the isovolumic blood-perfused dog heart.

Length dependence of activation studied in the isovolumic blood-perfused dog heart.

VEGF–PLCγ1 pathway controls cardiac contractility in the embryonic heart

Force-velocity relation and contractility in striated muscles.

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