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Endothelial Function in a Mouse Model of Myeloperoxidase Deficiency

Artikel i vetenskaplig tidskrift
Författare Veronika Golubinskaya
Ulla Brandt-Eliasson
Li-Ming Gan
Martin Kjerrulf
Holger Nilsson
Publicerad i Biomed Research International
Volym 2014
Nummer/häfte 128046
ISSN 2314-6133
Publiceringsår 2014
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Språk en
Länkar dx.doi.org/10.1155/2014/128046
Ämnesord CARDIOVASCULAR-DISEASE, NITRIC-OXIDE, ATHEROSCLEROSIS, DYSFUNCTION, MICE
Ämneskategorier Klinisk medicin

Sammanfattning

Myeloperoxidase (MPO) activity is suggested to reduce the function of vascular nitric oxide, thereby contributing to endothelial dysfunction, although data in rodents are inconclusive. We examined vascular contractile and relaxant responses in MPO-deficient (MPO-/-) and wild- type mice to investigate the role for myeloperoxidase in the development of endothelial dysfunction. Carotid and saphenous arteries were taken from 8-month-old mice and studied in a myograph. Responses of carotid arteries to phenylephrine, high potassium, or acetylcholine (Ach) were statistically not different from controls. Treatment with lipopolysaccharide (LPS; to enhance endothelial dysfunction) reduced responses to Ach in MPO-/- but did not affect responses in wild-type. In response to high concentrations of Ach, carotid arteries responded with transient contractions, which were not different between the groups and not affected by LPS treatment. Saphenous arteries from MPO-/- had smaller normalized diameters and developed less contractile force. Vessels from MPO-/- were less sensitive to Ach than controls. These data suggest that mature MPO-deficient mice do not show enhanced endothelial function compared to wild-type mice, even when provoked with LPS treatment. The EDHF response appears to be reduced in MPO deficiency.

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