Interactions between K+ and beta 2-adrenoreceptors in determining muscle vasodilatation induced in the rat by systemic hypoxia

R Mian, J M Marshall, P Kumar

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)

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 languageEnglish
Pages (from-to)407-10
Number of pages4
JournalExperimental Physiology
Volume75
Issue number3
Publication statusPublished - May 1990

Keywords

  • Animals
  • Anoxia
  • Blood Gas Analysis
  • Brachial Artery
  • Femoral Artery
  • Muscles
  • Oxygen
  • Potassium
  • Rats
  • Receptors, Adrenergic, beta
  • Sotalol
  • Vasodilation

Fingerprint

Dive into the research topics of 'Interactions between K+ and beta 2-adrenoreceptors in determining muscle vasodilatation induced in the rat by systemic hypoxia'. Together they form a unique fingerprint.

Cite this