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Interactions between K+ and beta 2‐adrenoreceptors in determining muscle vasodilatation induced in the rat by systemic hypoxia
Author(s) -
Mian R,
Marshall JM,
Kumar P
Publication year - 1990
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1990.sp003416
Subject(s) - dilator , hypoxia (environmental) , vasodilation , hindlimb , medicine , blockade , skeletal muscle , endocrinology , chemistry , propranolol , receptor , oxygen , organic chemistry
In spontaneously breathing anaesthetized rats, both moderate and severe hypoxia caused increases in [K+] in venous efflux from hindlimb muscle, from 4.3 to 4.6 and from 3.8 to 4.4 mM respectively; the increases were accentuated to 5.2 and 5.7 mM after beta 2‐receptor blockade with I.V. sotalol. Sotalol also potentiated the vasodilatation evoked in hindlimb muscle by moderate hypoxia, but reduced that evoked by severe hypoxia. We propose that K+ released from muscle during hypoxia contributed to the local vasodilatation. Further, we suggest that this effect was enhanced in moderate hypoxia by blockade of the beta 2‐mediated uptake mechanism for K+ in skeletal muscle, but outweighed in severe hypoxia by blockade of the beta 2‐mediated dilator action of circulating catecholamines on vascular muscle.