We evaluated endothelial function of thoracic aortas and pulmonary arteries
in a population of European wood mice (Apodemus sylvaticus), which
exhibits hypercholesteromia. According to the plasma cholesterol level,
mice were divided into two groups: hypercholesterolemic (AHL, total
plasma cholesterol 200-300 mg/dl) and normocholesterolemic (ANL, total
plasma cholesterol <200 mg/dl). Acetylcholine (ACh) caused
endothelium-dependent relaxation of precontracted aortas and pulmonary
arteries. Relaxation of the pulmonary artery is completely dependent on
nitric oxide. This relaxation was inhibited in AHL pulmonary arteries.
On the other hand, part of the ACh-induced relaxation of the thoracic aorta
was resistant to Nω-nitro-L-arginine (L-NNA). L-NNA-sensitive and
-resistant relaxation to ACh were also inhibited in AHL aortas. Inhibition
of endothelium-dependent relaxation of the aortas was correlated with total
plasma cholesterol level. Endothelium-independent relaxation to sodium
nitroprusside (SNP) was similar in AHL and ANL pulmonary arteries, but
in the thoracic aorta of AHL mice, the sensitivity to SNP was slightly
decreased, without a change in maximal response to SNP. No
morphological change was observed in the aortas and the pulmonary
arteries from AHL and ANL mice. Thus, AHL mice are valuable as a new
experimental model to study the relation of hyperlipidemia to vascular
disease since the endothelial function is impaired in these mild
hyperlipidemic animals.
リポジトリのご案内
Impairment of endothelium-dependent relaxation of aortas and pulmonary arteries from spontaneously hyperlipidemic mice (Apodemus sylvaticus)
VascPharmacol47_166.pdf
(184.28KB)
