Role of intracellular calcium handling in force-interval relationships of human ventricular myocardium.

Experiments were performed in human working myocardium to investigate the relationship of intracellular calcium handling and availability to alterations in the strength of contraction produced by changes in stimulation rate and pattern. Both control and myopathic muscles exhibited potentiation of peak isometric force during the postextrasystolic contraction which was associated with an increase in the peak intracellular calcium transient. Frequency-related force potentiation was attenuated in myopathic muscles compared to controls. This occurred despite an increase in resting intracellular calcium and in the peak amplitude of the calcium transient as detected with aequorin. Therefore, abnormalities in contractile function of myopathic muscles during frequency-related force potentiation are not due to decreased availability of intracellular calcium, but more likely reflect differences in myofibrillar calcium responsiveness. Sarcolemmal calcium influx may also contribute to frequency-related changes in contractile force in myopathic muscles as suggested by a decrease in action potential duration with increasing stimulation frequency which is associated with fluctuations in peak calcium transient amplitude.

[1]  J. Koch-weser.  Effect of rate changes on strength and time course of contraction of papillary muscle. , 1963, The American journal of physiology.

[2]  D. Noble,et al.  The dependence of plateau currents in cardiac Purkinje fibres on the interval between action potentials , 1972, The Journal of physiology.

[3]  A. Fabiato,et al.  Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells from cardiace and skeletal muscles. , 1978, The Journal of physiology.

[4]  J. C. Bailey,et al.  Alternans of Action Potential Duration After Abrupt Shortening of Cycle Length: Differences Between Dog Purkinje and Ventricular Muscle Fibers , 1988, Circulation research.

[5]  E. Lakatta,et al.  Intracellular calcium transients and developed tension in rat heart muscle. A mechanism for the negative interval-strength relationship , 1985, The Journal of general physiology.

[6]  F. Schoen,et al.  Deficient production of cyclic AMP: pharmacologic evidence of an important cause of contractile dysfunction in patients with end-stage heart failure. , 1987, Circulation.

[7]  J. R. Blinks,et al.  Field stimulation as a means of effecting the graded release of autonomic transmitters in isolated heart muscle. , 1966, The Journal of pharmacology and experimental therapeutics.

[8]  J. Peterson,et al.  Vanadate and phosphate ions reduce tension and increase cross-bridge kinetics in chemically skinned heart muscle. , 1981, Biochimica et biophysica acta.

[9]  W. Wier.  Calcium transients during excitation-contraction coupling in mammalian heart: aequorin signals of canine Purkinje fibers. , 1980, Science.

[10]  R. Shemin,et al.  The creatine kinase system in normal and diseased human myocardium. , 1985, The New England journal of medicine.

[11]  J KOCH-WESER,et al.  Analysis of the effects of changes in rate and rhythm upon myocardial contractility. , 1961, The Journal of pharmacology and experimental therapeutics.

[12]  E. Marbán,et al.  Relationship between force and intracellular [Ca2+] in tetanized mammalian heart muscle , 1986, The Journal of general physiology.

[13]  D. Allen,et al.  Oscillations of intracellular Ca2+ in mammalian cardiac muscle , 1983, Nature.

[14]  W. Wier,et al.  Intracellular calcium transients underlying the short‐term force‐interval relationship in ferret ventricular myocardium. , 1986, The Journal of physiology.

[15]  J. Gwathmey,et al.  Altered calcium handling in experimental pressure-overload hypertrophy in the ferret. , 1985, Circulation research.

[16]  R. Tsien,et al.  Inactivation of calcium channels in mammalian heart cells: joint dependence on membrane potential and intracellular calcium. , 1985, The Journal of physiology.

[17]  W Grossman,et al.  Alterations in left ventricular relaxation and diastolic compliance in congestive cardiomyopathy. , 1979, Cardiovascular research.

[18]  G. M. Briggs,et al.  Role of intracellular sodium in the regulation of intracellular calcium and contractility. Effects of DPI 201-106 on excitation-contraction coupling in human ventricular myocardium. , 1988, The Journal of clinical investigation.

[19]  E. Lakatta,et al.  Bimodal Effect of Stimulation on Light Fluctuation Transients Monitoring Spontaneous Sarcoplasmic Reticulum Calcium Release in Rat Cardiac Muscle , 1988, Circulation research.

[20]  J. Koch-weser,et al.  THE INFLUENCE OF THE INTERVAL BETWEEN BEATS ON MYOCARDIAL CONTRACTILITY. , 1963, Pharmacological reviews.

[21]  F. Schoen,et al.  Reversal of the force-frequency relationship in working myocardium from patients with end-stage heart failure , 1988 .

[22]  E. Kranias,et al.  Phosphorylation of C-protein, troponin I and phospholamban in isolated rabbit hearts. , 1988, The Biochemical journal.

[23]  W Grossman,et al.  Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure. , 1987, Circulation research.

[24]  D. Yue,et al.  Intracellular [Ca2+] related to rate of force development in twitch contraction of heart. , 1987, The American journal of physiology.

[25]  A. Schwartz,et al.  Rate of Calcium Binding and Uptake in Normal Animal and Failing Human Cardiac Muscle: MEMBRANE VESICLES (RELAXING SYSTEM) AND MITOCHONDRIA , 1969, Circulation research.

[26]  E. Lakatta,et al.  Spontaneous Sarcoplasmic Reticulum Calcium Release in Rat and Rabbit Cardiac Muscle: Relation to Transient and Rested‐State Twitch Tension , 1988, Circulation research.

[27]  E. Lakatta,et al.  Cellular calcium fluctuations in mammalian heart: direct evidence from noise analysis of aequorin signals in Purkinje fibers. , 1983, Proceedings of the National Academy of Sciences of the United States of America.

[28]  Norman R. Draper,et al.  Applied regression analysis (2. ed.) , 1981, Wiley series in probability and mathematical statistics.

[29]  K. Sagawa,et al.  Postextrasystolic Potentiation of the Isolated Canine Left Ventricle: Relationship to Mechanical Restitution , 1985, Circulation research.

[30]  A. A. Walker,et al.  Maximal Twitch Tension in Intact Length‐Clamped Ferret Papillary Muscles Evoked by Modified Postextrasystolic Potentiation , 1988, Circulation research.

[31]  A. Bassett,et al.  ATP-sensitive K+ channels are altered in hypertrophied ventricular myocytes. , 1988, The American journal of physiology.