Channel-mediated calcium current in the heart
- PMID: 2856472
- DOI: 10.1007/BF02125730
Channel-mediated calcium current in the heart
Abstract
Calcium ions play an important role in the regulation of heart functions. Calcium ions may enter or leave the myocardial cell through various mechanisms, including several exchange mechanisms and pumps. This review concentrates on the influx of calcium ions through channels in the sarcolemma, resulting in an electric current flow. The calcium current plays an important role in the maintenance of the action potential duration, in the generation of pacemaker activity, and in the initiation of contraction. The calcium current displays both activation and a subsequent inactivation when the membrane potential is changed in a stepwise fashion. Previously, the activation was thought to occur rather slowly, hence the name "slow inward current." Recent evidence suggests that the calcium current occurs much faster and that two types of calcium currents might exist, differing in their selectivity to other ions and in their sensitivity to membrane potential and to drugs. The calcium current is modulated by several factors. Beta-adrenergic stimulation increases the calcium current by increasing the opening probability of the calcium channel. The effects of acetylcholine are less well described. There also exists a class of drugs, called calcium channel blockers (or calcium antagonists) that decrease the flow of calcium ions through calcium channels. It is not quite clear how the calcium current is changed during myocardial ischemia. Factors that may reduce the calcium current during ischemia are the increased extracellular potassium concentration, metabolic inhibition and a decreased ATP level, and acidosis. Raised levels of intracellular cAMP, however, should lead to an increased calcium current.
Similar articles
-
Properties of calcium channels in cardiac muscle and vascular smooth muscle.Mol Cell Biochem. 1990 Dec 20;99(2):97-109. doi: 10.1007/BF00230339. Mol Cell Biochem. 1990. PMID: 1962848 Review.
-
Regulation of slow calcium channels of myocardial cells and vascular smooth muscle cells by cyclic nucleotides and phosphorylation.Mol Cell Biochem. 1994 Nov 23;140(2):103-17. doi: 10.1007/BF00926749. Mol Cell Biochem. 1994. PMID: 7898483 Review.
-
Ca2+ currents in compensated hypertrophy and heart failure.Cardiovasc Res. 1998 Feb;37(2):300-11. doi: 10.1016/s0008-6363(97)00273-3. Cardiovasc Res. 1998. PMID: 9614487 Review.
-
Mechanisms of cellular synchronization in the vascular wall. Mechanisms of vasomotion.Dan Med Bull. 2010 Oct;57(10):B4191. Dan Med Bull. 2010. PMID: 21040688 Review.
-
[Transmembrane inward currents during excitation of the heart (author's transl)].Klin Wochenschr. 1975 Dec 1;53(23):1089-99. doi: 10.1007/BF01614276. Klin Wochenschr. 1975. PMID: 1206966 German.
Cited by
-
Exosomal circRNA as a novel potential therapeutic target for multiple myeloma-related myocardial damage.Cancer Cell Int. 2021 Jun 13;21(1):311. doi: 10.1186/s12935-021-02011-w. Cancer Cell Int. 2021. PMID: 34120606 Free PMC article.
-
Pathophysiological Roles of the TRPV4 Channel in the Heart.Cells. 2023 Jun 17;12(12):1654. doi: 10.3390/cells12121654. Cells. 2023. PMID: 37371124 Free PMC article. Review.
-
Calcium Channels in the Heart: Disease States and Drugs.Cells. 2022 Mar 10;11(6):943. doi: 10.3390/cells11060943. Cells. 2022. PMID: 35326393 Free PMC article. Review.
-
Myocardial ischemia--metabolic pathways and implications of increased glycolysis.Cardiovasc Drugs Ther. 1990 Aug;4 Suppl 4:777-90. doi: 10.1007/BF00051275. Cardiovasc Drugs Ther. 1990. PMID: 1965525 Review.