Responses to ions and vasoconstrictor agents and changes of potassium fluxes in vascular smooth muscle during hypoxia
(1981) In Acta Physiologica Scandinavica 112(4). p.455-462- Abstract
- An inhibitory effect of hypoxia (Po2 less than 5 mmHg) on electrical and mechanical activity of the smooth muscle of the rat portal vein has been described by Hellstrand, Johansson & Norberg (1977). The present study using the sucrose gap method confirmed their finding that spontaneous activity was completely (or almost completely) abolished by the low Po2. Increased [K+]0 from 6 to 24 mM or decreased [Na+]0 from 137.5 to 76.5 mM reinitiated electrical and mechanical activity during hypoxia. If muscle activity had already been increased by 24 mM K+ or 76.5 mM Na+ solutions in the aerobic situation, switching to hypoxia caused only partial inhibition. In hypoxic solutions of such altered ionic composition a gradual increase in muscle... (More)
- An inhibitory effect of hypoxia (Po2 less than 5 mmHg) on electrical and mechanical activity of the smooth muscle of the rat portal vein has been described by Hellstrand, Johansson & Norberg (1977). The present study using the sucrose gap method confirmed their finding that spontaneous activity was completely (or almost completely) abolished by the low Po2. Increased [K+]0 from 6 to 24 mM or decreased [Na+]0 from 137.5 to 76.5 mM reinitiated electrical and mechanical activity during hypoxia. If muscle activity had already been increased by 24 mM K+ or 76.5 mM Na+ solutions in the aerobic situation, switching to hypoxia caused only partial inhibition. In hypoxic solutions of such altered ionic composition a gradual increase in muscle activity with time was seen especially in the low Na+-solution. Stimulating agents such as noradrenaline, acetylcholine, 4-aminopyridine, and Ba2+ could reinitiate spike activity and contractions under hypoxic conditions. Ouabain stimulated the activity in normoxia but no effect was seen in hypoxia. Uptake and washout of 42K+ was studied. No difference in uptake was found between normoxic and hypoxic conditions. The rate of 42K+ efflux was decreased under hypoxia. A similar decrease was produced by Mn2+ (0.4 mM) which, like hypoxia abolished phasic muscle activity. In both cases the reduction in 42K+ efflux may just reflect the elimination of action potentials. It is concluded from these results that profound hypoxia exerts its inhibitory effect on the smooth muscle to a large extent through membrane mechanisms responsible for pacemaker activity or spike generation. The electrophysiological response may be secondary to change in intracellular [Na+] or [Ca2+]. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1102887
- author
- Sigurdsson, S B ; Orlov, R S ; Hellstrand, Per LU and Johansson, B
- organization
- publishing date
- 1981
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Acta Physiologica Scandinavica
- volume
- 112
- issue
- 4
- pages
- 455 - 462
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:7315426
- scopus:0019415520
- ISSN
- 0001-6772
- language
- English
- LU publication?
- yes
- id
- 1e228146-08fc-4dd9-b017-f72f9146b016 (old id 1102887)
- date added to LUP
- 2016-04-01 16:09:30
- date last changed
- 2021-01-03 08:53:14
@article{1e228146-08fc-4dd9-b017-f72f9146b016,
abstract = {{An inhibitory effect of hypoxia (Po2 less than 5 mmHg) on electrical and mechanical activity of the smooth muscle of the rat portal vein has been described by Hellstrand, Johansson & Norberg (1977). The present study using the sucrose gap method confirmed their finding that spontaneous activity was completely (or almost completely) abolished by the low Po2. Increased [K+]0 from 6 to 24 mM or decreased [Na+]0 from 137.5 to 76.5 mM reinitiated electrical and mechanical activity during hypoxia. If muscle activity had already been increased by 24 mM K+ or 76.5 mM Na+ solutions in the aerobic situation, switching to hypoxia caused only partial inhibition. In hypoxic solutions of such altered ionic composition a gradual increase in muscle activity with time was seen especially in the low Na+-solution. Stimulating agents such as noradrenaline, acetylcholine, 4-aminopyridine, and Ba2+ could reinitiate spike activity and contractions under hypoxic conditions. Ouabain stimulated the activity in normoxia but no effect was seen in hypoxia. Uptake and washout of 42K+ was studied. No difference in uptake was found between normoxic and hypoxic conditions. The rate of 42K+ efflux was decreased under hypoxia. A similar decrease was produced by Mn2+ (0.4 mM) which, like hypoxia abolished phasic muscle activity. In both cases the reduction in 42K+ efflux may just reflect the elimination of action potentials. It is concluded from these results that profound hypoxia exerts its inhibitory effect on the smooth muscle to a large extent through membrane mechanisms responsible for pacemaker activity or spike generation. The electrophysiological response may be secondary to change in intracellular [Na+] or [Ca2+].}},
author = {{Sigurdsson, S B and Orlov, R S and Hellstrand, Per and Johansson, B}},
issn = {{0001-6772}},
language = {{eng}},
number = {{4}},
pages = {{455--462}},
publisher = {{Wiley-Blackwell}},
series = {{Acta Physiologica Scandinavica}},
title = {{Responses to ions and vasoconstrictor agents and changes of potassium fluxes in vascular smooth muscle during hypoxia}},
volume = {{112}},
year = {{1981}},
}