Impaired nitric oxide-mediated vasodilation in transgenic sickle mouse

Transgenic sickle mice expressing human beta(s)- and beta(s-Antilles)-globins show intravascular sickling, red blood cell adhesion, and attenuated arteriolar constriction in response to oxygen. We hypothesize that these abnormalities and the likely endothelial damage, also reported in sickle cell an...

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Bibliographic Details
Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 47; no. 6; pp. H1799 - H1806
Main Authors KAUL, D. K, LIU, X.-D, FABRY, M. E, NAGEL, R. L
Format Journal Article
LanguageEnglish
Published Bethesda, MD American Physiological Society 01.06.2000
Subjects
Anemias. Hemoglobinopathies
Biological and medical sciences
Cardiovascular disease
Diseases of red blood cells
Hematologic and hematopoietic diseases
Medical sciences
Rodents
Sickle cell anemia
Animal model
Endothelial cell
Sickle cell anemia
Arteriole
Transgenic animal
Hemopathy
Cremaster muscle
Vasodilation
Microcirculation
Vasomotricity
Hemolytic anemia
Arterial pressure
Hemoglobinopathy
Enzyme
Rodentia
Striated muscle
Gene expression
Nitric-oxide synthase
Genetic disease
Vertebrata
Mammalia
Mouse
Nitric oxide
Circulatory system
Hemodynamics
Oxidoreductases
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Summary:Transgenic sickle mice expressing human beta(s)- and beta(s-Antilles)-globins show intravascular sickling, red blood cell adhesion, and attenuated arteriolar constriction in response to oxygen. We hypothesize that these abnormalities and the likely endothelial damage, also reported in sickle cell anemia, alter nitric oxide (NO)-mediated microvascular responses and hemodynamics in this mouse model.
ISSN:0363-6135
1522-1539