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

doi:10.1161/01.RES.0000122044.21787.01

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 journal › Article › peer-review

109 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 language	English
Pages (from-to)	976-983
Number of pages	8
Journal	Circulation Research
Volume	94
Issue number	7
Early online date	12 Feb 2004
DOIs	https://doi.org/10.1161/01.RES.0000122044.21787.01
Publication status	Published - 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

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Access to Document

10.1161/01.RES.0000122044.21787.01

Cite this

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title = "Vasorelaxation by red blood cells and impairment in diabetes: Reduced nitric oxide and oxygen delivery by glycated hemoglobin",

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",

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TY - JOUR

T1 - Vasorelaxation by red blood cells and impairment in diabetes: Reduced nitric oxide and oxygen delivery by glycated hemoglobin

AU - James, Philip E.

AU - Lang, Derek

AU - Tufnell-Barret, Timothy

AU - Milsom, Alex B.

AU - Frenneaux, Michael P.

PY - 2004/4/16

Y1 - 2004/4/16

N2 - 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

AB - 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

KW - Animals

KW - Aorta, Thoracic

KW - Cell Hypoxia

KW - Diabetes Mellitus

KW - Endothelium, Vascular

KW - Erythrocytes

KW - Glycosylation

KW - Hemoglobin A, Glycosylated

KW - Hemoglobins

KW - Male

KW - Microcirculation

KW - Nitric Oxide

KW - Oxygen

KW - Phenylephrine

KW - Rabbits

KW - Triazenes

KW - Vasoconstrictor Agents

KW - Vasodilation

KW - omega-N-Methylarginine

U2 - 10.1161/01.RES.0000122044.21787.01

DO - 10.1161/01.RES.0000122044.21787.01

M3 - Article

C2 - 14963010

VL - 94

SP - 976

EP - 983

JO - Circulation Research

JF - Circulation Research

SN - 0009-7330

IS - 7

ER -