Korean J Physiol Pharmacol.
1998 Dec;2(6):705-714.
Moderate elevation of extracellular K+ concentration induces vasorelaxation in isolated rat, rabbit and human cerebral arteries: Role of Na pump and Ba-sensitive process
- Affiliations
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- 1Department of Physiology and Biophysics, Seoul National University College of Medicine, 28 Yongon-Dong, Chongno-Gu, Seoul 110-799, Korea.
- 2Department of Heart Research Institute, Seoul National University Medical Research Center, Korea.
- 3Department of Physiology, College of Medicine, Chungbuk National University, Cheongiu 361-763, Korea.
Abstract
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Cerebral blood vessels relax when extracellular K+ concentrations
((K+))e are elevated moderately (2~15 mM, K+-induced
vasorelaxation). We have therefore studied the underlying mechanism for
this K+-induced vasorelaxation in the isolated middle cerebral arteries
(MCAs). The effects of ouabain and Ba2+ on K+-induced vasorelaxation
were examined to determine the role of sodium pump and/or Ba-sensitive
process (possibly, inward rectifier K current) in the mechanism.
Mulvany myograph was used to study 24 rats, 18 rabbits, and 10 humans
MCAs (216+/-3 mum, 347+/-7 mum, and 597+/-39 mum in diameter when
stretched to a tension equivalent to 55 mmHg). High K+ (125 mM) and
PGF2alpha (1~10 muM) induced concentration-dependent contractions
in all 3 species, while histamine (10~50 muM) evoked contraction
only in the rabbits and induced relaxation in the rats and humans.
Addition of K+ (2~10 mM) to the control solution induced
vasorelaxations. These effects were inhibited by the pretreatment with
both ouabain (10 muM) and Ba2+ (0.1~0.3 mM) in the rat, but only
with ouabain (10 muM) in the rabbit and human. These results suggest
that K+-induced vasorelaxation occurs via the stimulation of
electrogenic Na pump in the rabbit and human MCAs, while in the rat
MCAs via the activation of both Na pump and Ba-sensitive process.