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.

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