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A link between adenosine, ATP‐sensitive K+ channels, potassium and muscle vasodilatation in the rat in systemic hypoxia.
Author(s) -
Marshall J M,
Thomas T,
Turner L
Publication year - 1993
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1993.sp019931
Subject(s) - vasodilation , adenosine , glibenclamide , medicine , chemistry , skeletal muscle , endocrinology , potassium channel , hypoxia (environmental) , oxygen , organic chemistry , diabetes mellitus
1. In anaesthetized rats, systemic hypoxia evoked hyperventilation, tachycardia, a fall in arterial pressure, vasodilatation in skeletal muscle and increases in K+ concentration measured in arterial plasma ([K+]a), venous efflux from muscle ([K+]v) and in right atrial plasma ([K+]at). The ATP‐sensitive potassium (K+ATP) channel inhibitor glibenclamide (10 or 20 mg kg‐1 i.v.) reduced the muscle vasodilatation and increase in [K+]v, but had no significant effect on the other changes. 2. The adenosine receptor antagonist, 8‐phenyltheophylline (8‐PT, 10 mg kg‐1 i.v.) had similar effects to glibenclamide. 3. Glibenclamide reduced the muscle vasodilatation evoked by the adenosine analogue, 2‐chloroadenosine given i.v. (30 micrograms kg‐1). 4. Infusion of adenosine (0.3 mg kg‐1 min‐1 for 5 min) into the hindlimb evoked muscle vasodilatation and an increase in [K+]v, both of which were abolished by 8‐PT. 5. We propose that during systemic hypoxia, part of the muscle vasodilatation that can be attributed to adenosine is due to the action of K+, which is released from skeletal muscle fibres through glibenclamide‐sensitive K+ channels (possibly K+ATP channels) that are activated by adenosine. This may be a general mechanism for the vasodilator influence of adenosine.