Vasorelaxation by red blood cells and impairment in diabetes: reduced nitric oxide and oxygen delivery by glycated hemoglobin

Philip E James, Derek Lang, Timothy Tufnell-Barret, Alex B Milsom, Michael P Frenneaux

Research output: Contribution to journalArticle

98 Citations (Scopus)

Abstract

Vascular dysfunction in diabetes is attributed to lack of bioavailable nitric oxide (NO) and is postulated as a primary cause of small vessel complications as a result of poor glycemic control. Although it has been proposed that NO is bound by red blood cells (RBCs) and can induce relaxation of blood vessels distal to its site of production in the normal circulation, the effect of RBC glycation on NO binding and relaxation of hypoxic vessels is unknown. We confirm RBC-induced vessel relaxation is inversely related to tissue oxygenation and is proportional to RBC S-nitrosohemoglobin (HbSNO) content (but not nitrosylhemoglobin content). We show more total NO bound inside highly glycated RBCs (0.0134 versus 0.0119 NO/Hb, respectively; P
Original languageEnglish
Pages (from-to)976-83
Number of pages8
JournalCirculation Research
Volume94
Issue number7
DOIs
Publication statusPublished - 16 Apr 2004

Keywords

  • Animals
  • Aorta, Thoracic
  • Cell Hypoxia
  • Diabetes Mellitus
  • Endothelium, Vascular
  • Erythrocytes
  • Glycosylation
  • Hemoglobin A, Glycosylated
  • Hemoglobins
  • Male
  • Microcirculation
  • Nitric Oxide
  • Oxygen
  • Phenylephrine
  • Rabbits
  • Triazenes
  • Vasoconstrictor Agents
  • Vasodilation
  • omega-N-Methylarginine

Cite this