Editorial: Electrical activity and excitation-contraction coupling in mammalian ventricular muscle.
The modern view of the mammalian ventricular action potential is that Na-ions are responsible for depolarization, the plateau is maintained by an inward Ca current and repolarization is due to the inactivation of this inward Ca current against a background outward K current. The electrical activity spreads over the surface and T-tubules of the cell and the inflow of Ca-ions, and possibly also the electrical signal, cause, a further release of Ca from internal stores, the lateral cisternae of the sarcoplasmic reticulum (SR). This released Ca, by triggering the splitting of ATP, induces contraction. The released Ca is pumped back into the longitudinal SR and, as the Ca concentration is reduced, relaxation occurs. The Ca in the longitudinal SR is transported back to the storage site in the cisternae. This completes the cycle, release, uptake, transport back to the releasing site. On the basis of this scheme, the action of various drugs is briefly discussed.
D000200:Action Potentials; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism / Q000502:physiology; D006321:Heart / Q000502:physiology*; D008322:Mammals / Q000502:physiology*; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D011188:Potassium / Q000378:metabolism / Q000502:physiology; D012519:Sarcoplasmic Reticulum / Q000502:physiology
D000255:Adenosine Triphosphate; D011188:Potassium; D002118:Calcium