Acute effects of glucose on reactivity of cerebral microcirculation: Role of activation of protein kinase C

W. G. Mayhan, K. P. Patel

Research output: Contribution to journalArticlepeer-review

64 Scopus citations


Our first goal was to determine whether acute hyperglycemia alters endothelium-dependent reactivity of rat cerebral arterioles. Our second goal was to investigate a possible mechanism for impaired reactivity during acute hyperglycemia. Diameter of pial arterioles was measured during suffusion with ADP, acetylcholine, histamine, N-methyl-D-aspartate (NMDA), and nitroglycerin before and during application of a suffusate containing D-glucose (5, 10, 20, and 25 mM). ADP, acetylcholine, histamine, NMDA, and nitroglycerin produced dose-related vasodilatation before application of D-glucose. Vasodilatation in response to the agonists was not altered by 5 and 10 mM D-glucose. In contrast, vasodilatation in response to ADP, acetylcholine, histamine, and NMDA was impaired during application of 20 and 25 mM D-glucose. Dilatation in response to nitroglycerin was not altered. Application of the protein kinase C inhibitor calphostin C (1.0 nM) or chelerythrine (10 nM) restored endothelium-dependent vasodilatation during application of 25 mM D-glucose. Thus acute hyperglycemia impairs endothelium-dependent responses of cerebral arterioles via the activation of protein kinase C.

Original languageEnglish (US)
Pages (from-to)H1297-H1302
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number4 38-4
StatePublished - 1995


  • N-methyl-D- aspartate
  • acetylcholine
  • adenosine diphosphate
  • brain
  • calphostin C
  • chelerythrine
  • endothelium-dependent dilation
  • histamine
  • hyperglycemia
  • nitroglycerin
  • rats

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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