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Contractures induced by reversed Na+/Ca2+ exchange in rat portal vein: effects of calcium antagonists

Johansson, B and Hellstrand, Per LU (1987) In Journal of Cardiovascular Pharmacology 10(Suppl. 1). p.75-81
Abstract
Spontaneous electrical and mechanical activity was abolished in isolated preparations of rat portal vein by exposure to K+-free Krebs solution. This procedure probably also increased the intracellular [Na+] owing to interference with the active transmembrane Na+-K+ transport. Contractures could be induced under these conditions by lowering extracellular [Na+] from the control level of 144 to 17 mM using sucrose, TrisCl, or LiCl as NaCl substitutes. Contractile force depended on the type of substitute: sucrose greater than TrisCl greater than LiCl. These contractures are thought to be caused by influx of extracellular Ca2+ through the Na+/Ca2+ exchanger, which otherwise transports Ca2+ in the opposite direction at normal transmembrane Na+... (More)
Spontaneous electrical and mechanical activity was abolished in isolated preparations of rat portal vein by exposure to K+-free Krebs solution. This procedure probably also increased the intracellular [Na+] owing to interference with the active transmembrane Na+-K+ transport. Contractures could be induced under these conditions by lowering extracellular [Na+] from the control level of 144 to 17 mM using sucrose, TrisCl, or LiCl as NaCl substitutes. Contractile force depended on the type of substitute: sucrose greater than TrisCl greater than LiCl. These contractures are thought to be caused by influx of extracellular Ca2+ through the Na+/Ca2+ exchanger, which otherwise transports Ca2+ in the opposite direction at normal transmembrane Na+ gradient. The contractile response to low Na+ was rapidly and completely abolished in nominally Ca2+-free medium; it was strongly inhibited by 0.4 mM MnCl2 but was not affected by high concentrations of the organic calcium antagonists, felodipine (10(-6) M), verapamil (10(-5) M), or diltiazem (10(-5) M). We conclude that the Na+/Ca2+-exchanger is an effective pathway for Ca2+ transport over vascular smooth muscle cell membrane; this pathway is not blocked by calcium antagonists. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Cardiovascular Pharmacology
volume
10
issue
Suppl. 1
pages
75 - 81
publisher
Lippincott Williams & Wilkins
external identifiers
  • pmid:2442524
  • scopus:0023256725
ISSN
1533-4023
language
English
LU publication?
yes
id
bf8ad8ed-47ca-4fce-ae71-ea4c983d956d (old id 1103923)
date added to LUP
2008-08-08 16:30:48
date last changed
2017-08-06 03:37:33
@article{bf8ad8ed-47ca-4fce-ae71-ea4c983d956d,
  abstract     = {Spontaneous electrical and mechanical activity was abolished in isolated preparations of rat portal vein by exposure to K+-free Krebs solution. This procedure probably also increased the intracellular [Na+] owing to interference with the active transmembrane Na+-K+ transport. Contractures could be induced under these conditions by lowering extracellular [Na+] from the control level of 144 to 17 mM using sucrose, TrisCl, or LiCl as NaCl substitutes. Contractile force depended on the type of substitute: sucrose greater than TrisCl greater than LiCl. These contractures are thought to be caused by influx of extracellular Ca2+ through the Na+/Ca2+ exchanger, which otherwise transports Ca2+ in the opposite direction at normal transmembrane Na+ gradient. The contractile response to low Na+ was rapidly and completely abolished in nominally Ca2+-free medium; it was strongly inhibited by 0.4 mM MnCl2 but was not affected by high concentrations of the organic calcium antagonists, felodipine (10(-6) M), verapamil (10(-5) M), or diltiazem (10(-5) M). We conclude that the Na+/Ca2+-exchanger is an effective pathway for Ca2+ transport over vascular smooth muscle cell membrane; this pathway is not blocked by calcium antagonists.},
  author       = {Johansson, B and Hellstrand, Per},
  issn         = {1533-4023},
  language     = {eng},
  number       = {Suppl. 1},
  pages        = {75--81},
  publisher    = {Lippincott Williams & Wilkins},
  series       = {Journal of Cardiovascular Pharmacology},
  title        = {Contractures induced by reversed Na+/Ca2+ exchange in rat portal vein: effects of calcium antagonists},
  volume       = {10},
  year         = {1987},
}