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Responses to ions and vasoconstrictor agents and changes of potassium fluxes in vascular smooth muscle during hypoxia

Sigurdsson, S B; Orlov, R S; Hellstrand, Per LU and Johansson, B (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)
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Contribution to journal
publication status
published
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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
2008-08-13 16:21:45
date last changed
2017-01-01 06:57:21
@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},
}