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This Article Full Text Full Text (PDF) All Versions of this Article: 289/4/H1710    most recent 00614.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Mo, F. M. Articles by Ballard, H. J. Search for Related Content PubMed PubMed Citation Articles by Mo, F. M. Articles by Ballard, H. J.

Acute systemic hypoxia elevates venous but not interstitial potassium of dog skeletal muscle

Department of Physiology, The University of Hong Kong, Pokfulam, Hong Kong

Submitted 21 June 2004 ; accepted in final form 11 May 2005

Potassium release through ATP-sensitive potassium (K_ATP) channels contributes to hypoxic vasodilation in the skeletal muscle vascular bed: It is uncertain whether K_ATP channels on muscle cells contribute to the process. Potassium from muscle cells must cross the interstitial space to reach the vascular tissues, whereas that from vascular endothelium would have a higher concentration in venous blood than in interstitial fluid. We determined the effect of systemic hypoxia on arterial, venous, and interstitial potassium in the constant-flow-perfused gracilis muscles of anesthetized dogs. Hypoxia reduced arterial PO₂ from 138 to 25 and PCO₂ from 28 to 26 mmHg. Arterial pH and potassium were well correlated (r² = 0.9): Both increased in early hypoxia and decreased during the postcontrol. In denervated muscles, perfusion pressure decreased from 95 to 76 mmHg by the end of the hypoxic period; neither venous nor interstitial potassium was elevated. In innervated muscles, perfusion pressure increased from 110 to 172 mmHg by the 11th min of hypoxia and then decreased to 146 mmHg by the end of the hypoxic period; venous potassium increased from 5.0 to 5.3 mM, but interstitial potassium remained unchanged. Glibenclamide abolished both the increase in venous potassium and the hypoxic vasodilation in the innervated muscle. Thus skeletal muscle cells were unlikely to have contributed to the release of potassium, which was suggested to originate from vascular endothelium. The sympathetic nerve supply may play a direct or indirect role in the opening of K_ATP channels under hypoxic conditions.