Abstract
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.
Original language | English |
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Pages (from-to) | 407-10 |
Number of pages | 4 |
Journal | Experimental Physiology |
Volume | 75 |
Issue number | 3 |
Publication status | Published - May 1990 |
Keywords
- Animals
- Anoxia
- Blood Gas Analysis
- Brachial Artery
- Femoral Artery
- Muscles
- Oxygen
- Potassium
- Rats
- Receptors, Adrenergic, beta
- Sotalol
- Vasodilation