Contractures induced by reversed Na+/Ca2+ exchange in rat portal vein: effects of calcium antagonists
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1103923
- author
- Johansson, B and Hellstrand, Per LU
- organization
- publishing date
- 1987
- 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
- 2016-04-01 11:56:15
- date last changed
- 2021-01-03 10:35:37
@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}},
}