Recent insights into the calcium channels

R. Zelis, R. Moore

Research output: Contribution to journalArticle

18 Citations (Scopus)

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 β1-adrenergic receptor stimulation. In vascular smooth muscle, the postjunctional α2-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 α1-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 β1-, α2-, or α1-adrenergic receptors.

Original languageEnglish (US)
Pages (from-to)IV-14-IV-16
JournalCirculation
Volume80
Issue number6 SUPPL.
StatePublished - Dec 1 1989

Fingerprint

Calcium Channels
Adrenergic Receptors
Calcium
Vascular Smooth Muscle
L Forms
Sarcoplasmic Reticulum
Type C Phospholipases
Inositol
Cardiovascular System
Cyclic AMP-Dependent Protein Kinases
GTP-Binding Proteins
Norepinephrine
Ions

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Zelis, R., & Moore, R. (1989). Recent insights into the calcium channels. Circulation, 80(6 SUPPL.), IV-14-IV-16.
Zelis, R. ; Moore, R. / Recent insights into the calcium channels. In: Circulation. 1989 ; Vol. 80, No. 6 SUPPL. pp. IV-14-IV-16.
@article{c74a794145d742bfa1f3632c69a84604,
title = "Recent insights into the calcium channels",
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 β1-adrenergic receptor stimulation. In vascular smooth muscle, the postjunctional α2-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 α1-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 β1-, α2-, or α1-adrenergic receptors.",
author = "R. Zelis and R. Moore",
year = "1989",
month = "12",
day = "1",
language = "English (US)",
volume = "80",
pages = "IV--14--IV--16",
journal = "Circulation",
issn = "0009-7322",
publisher = "Lippincott Williams and Wilkins",
number = "6 SUPPL.",

}

Zelis, R & Moore, R 1989, 'Recent insights into the calcium channels', Circulation, vol. 80, no. 6 SUPPL., pp. IV-14-IV-16.

Recent insights into the calcium channels. / Zelis, R.; Moore, R.

In: Circulation, Vol. 80, No. 6 SUPPL., 01.12.1989, p. IV-14-IV-16.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Recent insights into the calcium channels

AU - Zelis, R.

AU - Moore, R.

PY - 1989/12/1

Y1 - 1989/12/1

N2 - 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 β1-adrenergic receptor stimulation. In vascular smooth muscle, the postjunctional α2-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 α1-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 β1-, α2-, or α1-adrenergic receptors.

AB - 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 β1-adrenergic receptor stimulation. In vascular smooth muscle, the postjunctional α2-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 α1-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 β1-, α2-, or α1-adrenergic receptors.

UR - http://www.scopus.com/inward/record.url?scp=0024804901&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024804901&partnerID=8YFLogxK

M3 - Article

C2 - 2557177

AN - SCOPUS:0024804901

VL - 80

SP - IV-14-IV-16

JO - Circulation

JF - Circulation

SN - 0009-7322

IS - 6 SUPPL.

ER -

Zelis R, Moore R. Recent insights into the calcium channels. Circulation. 1989 Dec 1;80(6 SUPPL.):IV-14-IV-16.