Role of K+ in regulating hypoxic cerebral blood flow in the rat: effect of glibenclamide and ouabain.

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  • Author(s): Reid JM;Reid JM; Paterson DJ
  • Source:
    The American journal of physiology [Am J Physiol] 1996 Jan; Vol. 270 (1 Pt 2), pp. H45-52.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: American Physiological Society Country of Publication: United States NLM ID: 0370511 Publication Model: Print Cited Medium: Print ISSN: 0002-9513 (Print) Linking ISSN: 00029513 NLM ISO Abbreviation: Am J Physiol Subsets: MEDLINE
    • Publication Information:
      Publication: Bethesda, MD : American Physiological Society
      Original Publication: Washington [etc.] American Physiological Society.
    • Subject Terms:
      Cerebrovascular Circulation/*drug effects ; Glyburide/*pharmacology ; Hypoxia/*physiopathology ; Ouabain/*pharmacology ; Potassium/*physiology; Animals ; Blood Pressure ; Brain Ischemia/metabolism ; Extracellular Space/metabolism ; Female ; Hypercapnia/physiopathology ; Hyperoxia/physiopathology ; Male ; Osmolar Concentration ; Rats
    • Abstract:
      We assessed the role of extracellular potassium ([K+]e) on the increase in cerebral blood flow (CBF) during hypoxia, and we tested whether it was affected by glibenclamide or ouabain. Cortical CBF was measured using the hydrogen clearance technique in enflurane-anesthetized rats, and local [K+]e was measured with K+ microelectrodes adjacent to the hydrogen electrode. Eucapnic hypoxia (arterial Po2 approximately 35-40 Torr) increased CBF twofold and caused a modest rise in [K+]e (from 2.9 +/- 0.2 to 3.7 +/- 0.2 mM; mean arterial blood pressure, ABP, 86 +/- 5 mmHg). If ABP fell < 70 mmHg during hypoxia, no increase in CBF was seen, whereas [K+]e increased to > 20 mM. Glibenclamide (10-100 microM intracortically) attenuated [K+]e and CBF during hypoxia (ABP approximately 75 mmHg, P < 0.01). Ouabain (20-1,000 microM) increased [K+]e; however, it did not remove the hypoxic-induced rise in [K+]e. We conclude that glibenclamide-sensitive potassium channels contribute to the accumulation of [K+]e during hypoxia, although an increase in CBF during hypoxia can occur without a marked rise in [K+]e. Furthermore, if ABP falls below the lower limit of autoregulation during hypoxia, there is no increase in CBF, yet there is a large increase in [K+]e.
    • Accession Number:
      5ACL011P69 (Ouabain)
      RWP5GA015D (Potassium)
      SX6K58TVWC (Glyburide)
    • Publication Date:
      Date Created: 19960101 Date Completed: 19961220 Latest Revision: 20171213
    • Publication Date:
      20240829
    • Accession Number:
      10.1152/ajpheart.1996.270.1.H45
    • Accession Number:
      8769733