The effects of muscle length on intracellular calcium transients in mammalian cardiac muscle.

Allen, David G.; Kurihara, Satoshi

doi:10.1113/jphysiol.1982.sp014221

Cited by 533 publications

(405 citation statements)

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“…The slow secondary response to stretch is called SFR. 19 The SFR is associated with an increase in Ca 2+ handling due to a stretch-induced increase in Na + influx, followed by extrusion of Na + accompanied by Ca 2+ influx via the Na + /Ca 2+ exchanger. 29 Length-dependent activation of SACs cannot explain SIE and SFR simultaneously by itself because, as shown in Figure 4, SIE usually requires a substantial current to increase the membrane potential to the threshold level.…”

Section: Discussionmentioning

confidence: 99%

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Role of Sarcolemmal BKCa Channels in Stretch-Induced Extrasystoles in Isolated Chick Hearts

Iribe

Jin

Naruse

2011

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp echanical stress affects various aspects of cardiovascular physiology. 1-4 In particular, mechanically induced disturbance of heart rhythm is a phenomenon known as mechanoelectric feedback (MEF). 2,5 For instance, a mechanical blunt impact to the chest can initiate life-threatening arrhythmia, known as commotio cordis. 2 A precordial thump can also effectively terminate ventricular tachycardia and fibrillation. 4 These mechanosensitive responses in heart rhythm are believed to be caused by activation of cation-selective stretchactivated channels (SACs). In a cross-circulated isolated canine heart, acute diastolic left ventricular (LV) wall stretch induced an extrasystolic beat that could be suppressed by Gd 3+ , a potent (but non-specific) SAC blocker. 6 Furthermore, in a Langendorff-perfused rabbit heart, stretch-induced atrial fibrillation could be suppressed by Grammostola spatulata mechanotoxin 4 (GsMTx4), an SAC blocker. 7 Although these findings strongly suggest the involvement of SAC in stretchinduced arrhythmia, it has also been reported that many stretch-sensitive channels are K + or anion selective, 8-10 and their activation may stabilize membrane potential. Therefore, interactions between stretch-induced "destabilizer" and "stabilizer" channels need to be studied carefully to clarify the underlying mechanism of mechanically induced disturbance of heart rhythm.We have previously reported the electrophysiological properties of stretch-activated BKCa (SAKCa) channels cloned from cultured chick embryo ventricular myocytes. This type of channel is a voltage-sensitive K + channel, which is activated by intracellular Ca 2+ ([Ca 2+ ]i) and membrane stretch. 9 We found that an SAKCa channel is a splicing variant of a BKCa channel, and includes a stress axis-regulated exon (STREX) sequence, which is responsible for its stretch sensitivity. 11 Furthermore, we found that STREX variants of BKCa channels in chicks and humans share a short amino acid residue sequence (ERA) and show stretch sensitivity. STREX variants of these channels, however, in mice and rabbits that do not have the ERA sequence do not show stretch sensitivity. 11 Although it is widely believed that sarcolemmal BKCa channels do not exist in mature ventricular myocytes, 12 we reported the existence of sarcolemmal BKCa channels using direct micrographic evidence in post-hatch chick ventricular myocytes. Role of Sarcolemmal BKCa Channels in Stretch-Induced Extrasystoles in Isolated Chick HeartsGentaro Iribe, MD, PhD; Honghua Jin, PhD; Keiji Naruse, MD, PhDBackground: It remains unclear whether sarcolemmal BKCa channels in post-hatch chick ventricular myocytes contribute to stretch-induced extrasystoles (SIE), and whether they are stretch-activated BKCa (SAKCa) channels or a non-stretch-sensitive BKCa variant.

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Section: Discussionmentioning

confidence: 99%

“…The parameters for calculating fstretch_length are the same as in the original Oxsoft model 16 except for reduced gain (0.01), used to reproduce the results in our previous single cell study, 13 and slow force response (SFR) to stretch. 19 The final stretchdependent activation factor ( fstretch) was calculated as follows:…”

Section: Experiments Protocolmentioning

confidence: 99%

Role of Sarcolemmal BKCa Channels in Stretch-Induced Extrasystoles in Isolated Chick Hearts

Iribe

Jin

Naruse

2011

Circ J

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“…20 Length-dependent changes in the affinity of contractile proteins for calcium ions 21 or in the amount of calcium release 22 have a positive inotropic effect, whereas the uncoupling effects of shortening, viscoelastic properties, or length-dependent changes in transsarcolemmal kinetics of calcium have a negative inotropic effect. [23][24][25][26] Thus, the time course of the elastance curve could also be modulated when the loading condition is altered over a wide range.…”

Section: Load Dependence Of the Time-varying Elastance Curvementioning

confidence: 99%

Single-Beat Estimation of End-Systolic Elastance Using Bilinearly Approximated Time-Varying Elastance Curve

et al. 2000

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Background-Although left ventricular end-systolic elastance (E es ) has often been used as an index of contractility, technical difficulties in measuring volume and in changing loading conditions have made its clinical application somewhat limited. By approximating the time-varying elastance curve by 2 linear functions (isovolumic contraction phase and ejection phase) and estimating the slope ratio of these, we developed a method to estimate E es on a single-beat basis from pressure values, systolic time intervals, and stroke volume. Methods and Results-In 11 anesthetized dogs, we compared single-beat E es with that obtained with caval occlusion.Although the decrease (but not the increase) in contractility (5.3 to 11.4 mm Hg/mL) and the change in loading conditions (3.7 to 34.0 mm Hg/mL) over wide ranges significantly altered the slope ratio, the estimation of E es was reasonably accurate (yϭ0.97xϩ0.46, rϭ0.929, SEEϭ2.1 mm Hg/mL). Conclusions-E es can be estimated on a single-beat basis from easily obtainable variables by approximating the time-varying elastance curve by a bilinear function.

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“…The association TnC/Ca 2+ represents a fundamental event in muscle contraction; therefore, the sensitivity of TnC to Ca 2+ will be discussed in greater detail. This choice, furthermore, comes from studies shewing that myocardial force changes due to muscle length are unrelated to [Ca 2+ ] i 9,10 . The present article contains a review of studies related to the dependence of force and, more importantly, of the process of myocardial muscle activation on muscle length.…”

Section: The Degree Of Activation Of Cardiac Muscle Depends On Musclementioning

confidence: 99%

The degree of activation of cardiac muscle depends on muscle length

Rassier¹

2000

Arq. Bras. Cardiol.

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The Frank-Starling mechanism of the heart 1-3 can be described as the relationship between force and length of cardiac muscle. With the advent of the cross bridge theory of muscle contraction 4,5 and Gordon and collaborator's classical study 6 describing the fitting of this theory to the force-length relationship in skeletal muscle, several investigators started to study this relationship in cardiac muscle.The force-length relation in cardiac muscle is observed in a small variety of sarcomere lengths, between approximately 1.8 µm and 2.3 µm. This region corresponds to the ascending limb of the force-length relation of skeletal-muscle 6 . The force levels of the myocardium vary from zero at 1.8 µm to maximal force values at 2.3 µm. This large variation in force results in a very sleep force-length relation, especially when compared with this relation in skeletal muscle ( fig. 1). To get an idea, when the tension developed by the myocardium at different sarcomere lengths is normalized in relation to its maximal force (F max ) at the point where maximal length (L max ) occurs, the developed tension is approximately 10-15% when the myocardium is measured at 80% L max . Yet in skeletal muscle, normalized force is approximately 80-85% of F max 7 under the same conditions ( fig.1).This difference between skeletal and cardiac muscle shows that the force-length relationship in the myocardium are not a simple function of the degree of superposition of actin and myosin filaments. Because their lengths are similar in both muscles, other factors must be involved in the muscle force-length relationship. During recent years, this difference has been attributed to the dependence of muscle activation on sarcomere length 8 .Muscle activation has been used collectively in the literature to refer to various processes able to initiate muscle contraction, modifying the muscle state from "inactive" to "active". Thus, muscle activation has been associated with the frequency of muscle stimulation or membrane action potentials with intracellular Ca 2+ concentration [Ca 2+ ] i , or the occupation of the protein troponin C (TnC) by Ca 2+ . In this article, the term muscle contraction will be utilized to describe the proportion of TnC associated with Ca 2+ . The association TnC/Ca 2+ represents a fundamental event in muscle contraction; therefore, the sensitivity of TnC to Ca 2+ will be discussed in greater detail. This choice, furthermore, comes from studies shewing that myocardial force changes due to muscle length are unrelated to [Ca 2+ ] i 9,10 . The present article contains a review of studies related to the dependence of force and, more importantly, of the process of myocardial muscle activation on muscle length. In particular, the article intends to investigate mechanisms responsible for the dependence of the sensitivity of filaments to Ca 2+ on muscle length, as proposed in the literature.Dependence of the sensitivity of filaments to Ca 2+ on muscle length -Evidence that the activation of the myocardium is dependent on muscle lengt...

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The effects of muscle length on intracellular calcium transients in mammalian cardiac muscle.

Cited by 533 publications

References 18 publications

Role of Sarcolemmal BKCa Channels in Stretch-Induced Extrasystoles in Isolated Chick Hearts

Role of Sarcolemmal BKCa Channels in Stretch-Induced Extrasystoles in Isolated Chick Hearts

Single-Beat Estimation of End-Systolic Elastance Using Bilinearly Approximated Time-Varying Elastance Curve

The degree of activation of cardiac muscle depends on muscle length

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