Influence of V1 and V3 isomyosins on the mechanical behaviour of rat papillary muscle as studied by pseudo-random binary noise modulated length perturbations

Rossmanith, G. H.; Hoh, Joseph F. Y.; Kirman, A.; Kwan, Lee Jong

doi:10.1007/bf01753651

Cited by 75 publications

(52 citation statements)

References 42 publications

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“…The measured CCR was 2 73 + 0 11 Hz (N = 4) at 30°C, and was accordingly compatible with the CCR at 20°C in Ba2+ contracture (1-0 Hz;Saeki, Kawai & Zhao, 1991), based on the fact that the temperature coefficient, Qlo, of CCR is considered to be 3 3 (18-31°C) in cardiac muscle containing myosin isozyme V3 (Rossmanith, Hoh, Kirman & Kwan, 1986), and ferret cardiac muscle predominantly consists of myosin isozyme V3 (MacKinnon, Gwathmey, Allen, Briggs & Morgan, 1988). ,?-Adrenoceptor stimulation increased the CCR, as reported by Hoh et al (1988) and others (Berman et al 1988;Saeki et al 1990), and muscarinic receptor stimulation by ACh and carbachol restored the increased CCR (Fig.…”

Section: Changes In Cross-bridge Cycling Rate By Iso and A Chsupporting

confidence: 78%

Alterations in contractile properties and Ca2+ transients by beta‐and muscarinic receptor stimulation in ferret myocardium.

Hongo

Tanaka

Kurihara

1993

The Journal of Physiology

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SUMMARY1. To clarify the mechanism which regulates the time course of twitch tension when /1-and muscarinic receptors are stimulated, intracellular Ca2+ transients, Ca21 sensitivity of the contractile element and the cross-bridge cycling rate (CCR) were measured in ferret ventricular muscles. 4. In order to measure CCR, the perturbation analysis method was applied to steady-state tension of tetanic contraction. The CCR was not altered even when the tetanic tension level was decreased to 50 % by decreasing [Ca2+]0. Iso (0-1 taM) slightly decreased the tetanic tension level and increased the CCR from 2 73 to 3 25 Hz. The effect of Iso was observed when the Iso-decreased tension was recovered by an increase in [Ca2+]i. The addition of ACh (1 /tM) recovered the CCR which was increased by Iso, to the control level. Atropine (10 yM) blocked the effect of ACh, and carbachol (1 /tM) restored the CCR increased by Iso to the control level.5. The time course of Ca21 transients, Ca2+ sensitivity and CCR were antagonistically regulated by fl-and muscarinic receptor stimulation, but the time course of tension did not parallel the changes in these parameters. Therefore, these results suggest that the time course of tension, particularly the relaxation time, is not determined by the time course of Ca2+ transients, Ca2+ sensitivity and the CCR, and that other factors might be involved in the regulation of the time course of tension when /3-and muscarinic receptors are stimulated.S98 26

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Section: Changes In Cross-bridge Cycling Rate By Iso and A Chsupporting

confidence: 78%

Alterations in contractile properties and Ca2+ transients by beta‐and muscarinic receptor stimulation in ferret myocardium.

Hongo

Tanaka

Kurihara

1993

The Journal of Physiology

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“…For example, results from steady-state sinusoidal forcings or from approximation of the steady state with continuous changing frequency (13,26) or from frequency analysis of responses to pseudorandom binary sequence perturbations (13,25,30) can be presented in model-independent format as complex stiffness frequency spectra. However, interpretations of such results must eventually rely on some understanding of the system, i.e., a model.…”

Section: Advantagesmentioning

confidence: 99%

Interpreting cardiac muscle force-length dynamics using a novel functional model

Campbell

Chandra²,

Kirkpatrick³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

173

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. Interpreting cardiac muscle force-length dynamics using a novel functional model. Am J Physiol Heart Circ Physiol 286: H1535-H1545, 2004; 10.1152/ ajpheart.01029.2003.-To describe the dynamics of constantly activated cardiac muscle, we propose that length affects force via both recruitment and distortion of myosin cross bridges. This hypothesis was quantitatively tested for descriptive and explanative validity. Skinned cardiac muscle fibers from animals expressing primarily ␣-myosin heavy chain (MHC) (mouse, rat) or ␤-MHC (rabbit, ferret) were activated with solutions from pCa 6.1 to 4.3. Activated fibers were subjected to small-amplitude length perturbations [⌬L(t)] rich in frequency content between 0.1 and 40 Hz. In descriptive validation tests, the model was fit to the ensuing force response [⌬F(t)] in the time domain. In fits to 118 records, the model successfully accounted for most of the measured variation in ⌬F(t) (R 2 range, 0.997-0.736; median, 0.981). When some residual variations in ⌬F(t) were not accounted for by the model (as at low activation), there was very little coherence (Ͻ0.5) between these residual force variations and the applied ⌬L(t) input function, indicating that something other than ⌬L(t) was causing the measured variation in ⌬F(t). With one exception, model parameters were estimated with standard errors on the order of 1% or less. Thus parameters of the recruitment component of the model could be uniquely separated from parameters of the distortion component of the model and parameters estimated from any given fiber could be considered unique to that fiber. In explanative validation tests, we found that recruitment and distortion parameters were positively correlated with independent assessments of the physiological entity they were assumed to represent. The recruitment distortion model was judged to be valid from both descriptive and explanative perspectives and is, therefore, a useful construct for describing and explaining dynamic force-length relationships in constantly activated cardiac muscle. muscle stiffness; cross-bridge recruitment; cross-bridge distortion; model validation; mouse; rat; ferret; rabbit MUSCLE LENGTH modulates cardiac muscle force development, and the resultant force-length relationship (FLR) is basic to the Frank-Starling mechanism of the heart. In general, however, muscle FLRs extend beyond the typical isometric twitching conditions under which force-length data are commonly collected to also include the force response to any length change during contraction. Thus descriptors of muscle FLR should also depict the dynamic force response to length changes that occur during contraction. One often-studied aspect of the dynamic FLR is the force response to sinusoidal length change in a constantly activated muscle fiber. Under these dynamic conditions, the amplitude and phase of the force response depends on both the frequency and amplitude of the sinusoidal length change. Dividing the steady-state sinusoidal force response by the sinusoidal length change yields...

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“…A detailed description of the mechanical apparatus and temperature control is given in a previous paper (Rossmanith, Hoh, Kirman & Kwan, 1986). All experiments were carried out at 25°C.…”

Section: Mechanical Apparatus and Temperature Controlmentioning

confidence: 99%

Mechanism of action of endothelin in rat cardiac muscle: cross‐bridge kinetics and myosin light chain phosphorylation

Rossmanith

Hoh

Turnbull

et al. 1997

The Journal of Physiology

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The molecular mechanism of inotropic action of endothelin was investigated in rat ventricular muscle by studying its effects on characteristics of isometric twitch, barium‐induced steady contracture and the level of incorporation of 32Pi into myosin light chain 2. Exposure of rat papillary muscle to endothelin caused an increase in isometric twitch force but did not alter the twitch‐time parameters. Endothelin did not significantly change the maximum contracture tension but did cause an increase in contracture tension at submaximal levels of activation, without changes in the tension‐to‐stiffness ratio and kinetics of attached cross‐bridges. Kinetics of attached cross‐bridges were deduced during steady contracture from complex‐stiffness values, and in particular from the frequency at which muscle stiffness assumes a minimum value, fmin. Endothelin did not alter fmin. Endothelin caused an increase in the level of incorporation of 32Pi into myosin light chain 2 without a concurrent change in the level of incorporation of 32Pi into troponin I. We conclude that the inotropic action of endothelin is not due to an increase in the kinetics of attached cross‐bridges, nor due to a change in the force per unit cross‐bridge, but may result from an increased divalent cation sensitivity caused by elevated myosin light chain 2 phosphorylation, resembling post‐tetanic potentiation in fast skeletal muscle fibres.

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Influence of V1 and V3 isomyosins on the mechanical behaviour of rat papillary muscle as studied by pseudo-random binary noise modulated length perturbations

Cited by 75 publications

References 42 publications

Alterations in contractile properties and Ca2+ transients by beta‐and muscarinic receptor stimulation in ferret myocardium.

Alterations in contractile properties and Ca2+ transients by beta‐and muscarinic receptor stimulation in ferret myocardium.

Interpreting cardiac muscle force-length dynamics using a novel functional model

Mechanism of action of endothelin in rat cardiac muscle: cross‐bridge kinetics and myosin light chain phosphorylation

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