Voltage-gated calcium channel

Two-pore channel
Identifiers
SymbolTPC
PfamPF08473
OPM superfamily8
OPM protein6c96
Membranome214
Available protein structures:
Pfam  structures / ECOD  
PDBRCSB PDB; PDBe; PDBj
PDBsumstructure summary

Voltage-gated calcium channels (VGCCs), also known as voltage-dependent calcium channels (VDCCs), are a group of voltage-gated ion channels found in the membrane of excitable cells (e.g., muscle, glial cells, neurons, etc.) with a permeability to the calcium ion Ca2+.[1][2] These channels are slightly permeable to sodium ions, so they are also called Ca2+–Na+ channels, but their permeability to calcium is about 1000-fold greater than to sodium under normal physiological conditions.[3]

At physiologic or resting membrane potential, VGCCs are normally closed. They are activated (i.e.: opened) at depolarized membrane potentials and this is the source of the "voltage-gated" epithet. The concentration of calcium (Ca2+ ions) is normally several thousand times higher outside the cell than inside. Activation of particular VGCCs allows a Ca2+ influx into the cell, which, depending on the cell type, results in activation of calcium-sensitive potassium channels, muscular contraction,[4] excitation of neurons, up-regulation of gene expression, or release of hormones or neurotransmitters.

VGCCs have been immunolocalized in the zona glomerulosa of normal and hyperplastic human adrenal, as well as in aldosterone-producing adenomas (APA), and in the latter T-type VGCCs correlated with plasma aldosterone levels of patients.[5] Excessive activation of VGCCs is a major component of excitotoxicity, as severely elevated levels of intracellular calcium activates enzymes which, at high enough levels, can degrade essential cellular structures.

  1. ^ Catterall WA, Perez-Reyes E, Snutch TP, Striessnig J (December 2005). "International Union of Pharmacology. XLVIII. Nomenclature and structure-function relationships of voltage-gated calcium channels". Pharmacological Reviews. 57 (4): 411–25. doi:10.1124/pr.57.4.5. PMID 16382099. S2CID 10386627.
  2. ^ Yamakage M, Namiki A (February 2002). "Calcium channels--basic aspects of their structure, function and gene encoding; anesthetic action on the channels--a review". Canadian Journal of Anaesthesia. 49 (2): 151–64. doi:10.1007/BF03020488. PMID 11823393.
  3. ^ Hall JE (2011). Guyton and Hall Textbook of Medical Physiology with Student Consult Online Access (PDF) (12th ed.). Philadelphia: Elsevier Saunders. p. 64. ISBN 978-1-4160-4574-8. Archived from the original (PDF) on 2011-05-16. Retrieved 2011-03-22.
  4. ^ Wilson DP, Susnjar M, Kiss E, Sutherland C, Walsh MP (August 2005). "Thromboxane A2-induced contraction of rat caudal arterial smooth muscle involves activation of Ca2+ entry and Ca2+ sensitization: Rho-associated kinase-mediated phosphorylation of MYPT1 at Thr-855, but not Thr-697". The Biochemical Journal. 389 (Pt 3): 763–74. doi:10.1042/BJ20050237. PMC 1180727. PMID 15823093.
  5. ^ Felizola SJ, Maekawa T, Nakamura Y, Satoh F, Ono Y, Kikuchi K, Aritomi S, Ikeda K, Yoshimura M, Tojo K, Sasano H (October 2014). "Voltage-gated calcium channels in the human adrenal and primary aldosteronism". The Journal of Steroid Biochemistry and Molecular Biology. 144 Pt B (part B): 410–6. doi:10.1016/j.jsbmb.2014.08.012. PMID 25151951. S2CID 23622821.

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