Cardiac Muscle: The Regulation Of Excitation And Contraction

Contributors

Preface


1. Ionic Currents Underlying Cardiac Pacemaker Activity: A Summary of Voltage-Clamp Data from Single Cells

I. Foreword

II. Introduction

III. Methods

IV. Results

V. Summary

References


2. Inactivation and Modulation of Cardiac Ca Channels

I. Introduction

II. Inactivation of Cardiac Calcium Channels: Voltage- and Calcium-Mediated Mechanisms

III. State-Dependent Modulation of Ca-Channel Current

IV. Summary

References


3. Negative Surface Charge: Its Identification and Regulation of Cardiac Electrogenesis

I. Introduction

II. Fixed Negative Charges on the Surface of Cardiac Myocytes

III. Identification of the Negative Surface Charge

IV. Summary

References


4. Mechanisms of β-Adrenergic and Cholinergic Control of Ca and K Currents in the Heart

I. Introduction

II. Action Potential and Membrane Current

III. β-Adrenergic Stimulation

IV. Single-Ca-Channel Activity, Adrenaline, and cAMP

V. Mechanism of Action of Acetylcholine

VI. The Second Muscarinic Response

VII. Summary and Perspectives for Future Research

References


5. Modulation of Cell Electrical Properties by Peptide Hormones

I. Introduction

II. The Brain-Gut Peptides

III. The Polypeptide Growth Factors

IV. Mechanism of Peptide Hormone Action

V. Conclusions and Future Research Directions

References


6. Sodium-Calcium Exchange and Its Role in Generating Electric Current

I. Introduction

II. Equilibrium and Steady-State Theory of the Sodium-Calcium Exchange Process

III. Theory of Transient Changes in the Sodium-Calcium Exchange Process

IV. The Calcium Transient

V. The Sodium-Potassium Exchange Process

VI. Variation of E-NaCa during Activity

VII. How Much Current Should the Carrier Generate?

VIII. Time Constant for Exchange Process

IX. Ionic Currents That Might be Attributed to Sodium-Calcium Exchange

X. Relation between Slow Components of isi and the Transient Inward Current, iT1

XI. Artificially Induced Slow Inward Current

XII. Current-Voltage Relations for [Ca]i-Induced Variations in i-NaCa

XIII. Conclusions

References


7. Some Experimental Studies of Na-Ca Exchange in Heart Muscle

I. Introduction

II. Experimental Studies

III. Discussion

IV. Summary

References


8. The Regulation of Tension in Heart Muscle by Intracellular Sodium

I. Introduction

II. Methods

III. Results and Discussion

IV. Conclusions

References


9. Cardiac Glycosides: Regulation of Force and Rhythm

I. Introduction

II. Cardiac Glycosides and the Regulation of Contractile Force

III. Cardiac Glycosides and the Regulation of Rhythm

IV. Conclusions

References


10. Calcium at the Sarcolemma: Its Role in Control of Myocardial Contraction

I. Introduction

II. Extracellular Calcium

III. Sarcolemmal Calcium Binding

IV. Role of Phospholipid in Ca Binding

V. Relationship of Ca Binding to Primary Alteration in Transsarcolemmal Flux

VI. Present Concepts

VII. Conclusions

References


11. Release of Calcium from the Sarcoplasmic Reticulum

I. Introduction

II. Evidence for and against a Release of Calcium from the Sarcoplasmic Reticulum during Cardiac Excitation-Contraction Coupling

III. Hypothesis of Calcium-Induced Release of Calcium from the Sarcoplasmic Reticulum

IV. Hypothesis of Depolarization-Induced Release of Calcium from the Sarcoplasmic Reticulum

V. Hypothesis of Sodium-Induced Release of Calcium from the Sarcoplasmic Reticulum

VI. Hypothesis of Release of Calcium from the Sarcoplasmic Reticulum Induced by a Change in pH

VII. Hypothesis of Release of Calcium Induced by Movement of Transverse Tubular or Sarcolemmal Charged Particles Linked Mechanically to Sites in the Sarcoplasmic Reticular Membrane

VIII. Hypothesis of Release of Calcium from the Sarcoplasmic Reticulum Induced by Inositol (1,4,5)-Trisphosphate

References


12. Calcium-Binding Proteins in the Regulation of Muscle Contraction

I. Introduction

II. Calcium Channels

III. Calmodulin and Troponin C

IV. Similarities between the Calcium-Binding Proteins of the Contractile Apparatus (Troponin C and Calmodulin) and the Calcium Channel

V. The Na+ - Ca2+ Antiporter as a Calcium-Binding Protein That Controls Muscle Contraction

VI. Conclusions

References

Index