Referenced in: none

Automatically associated channels: Kir2.3 , Slo1

Title: Recent insights into the calcium channels.

Authors: R Zelis, R Moore

Journal, date & volume: Circulation, 1989 Dec , 80, IV14-6

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/2557177

Abstract
Calcium channels play a central role in the regulation of intracellular calcium (Ca2+) concentration, and their function is subject to control by voltage-regulated, receptor-regulated, or voltage- and receptor-regulated mechanisms. Three types of calcium channels have been described. These are the T (transient or "fast"), the N (neuronal), and the L (long lasting or "slow") channels. The L channels appear to be heterogeneous and have different properties in different tissues. Intracellular calcium-ion concentration can be increased by three types of receptor mechanisms. In the heart, L channels can be phosphorylated by a cyclic AMP-dependent protein kinase after beta 1-adrenergic receptor stimulation. In vascular smooth muscle, the postjunctional alpha 2-adrenergic receptor is coupled to a Ca2+ channel by a G protein; receptor stimulation facilitates calcium influx. This channel might be a form of L channel. A third receptor mechanism, especially active in vascular smooth muscle, is typified by the alpha 1-adrenergic receptor that, when stimulated, will activate phospholipase C. This leads to an increase in intracellular inositol trisphosphate (IP3), which is an intracellular messenger that can induce calcium release from the sarcoplasmic reticulum. Thus, release of norepinephrine from sympathetic nerves in the cardiovascular system stimulates the heart and vessels to contract by increasing Ca2+; however, the mechanism by which this occurs is different, depending on whether the noradrenergic agonist interacts with beta 1-, alpha 2-, or alpha 1-adrenergic receptors.