1. Vasomotor function of the vascular endothelium was examined in @entity1 subcutaneous arteries excised from 8 hypercholesterolaemic and 7 normolipidaemic subjects. 2. Left gluteal skin biopsies were performed under local anaesthesia. Subcutaneous arteries were isolated and two vessels from each subject mounted in separate myographs. A 20 ml fasting blood sample was taken at the time of the biopsy. 3. Hypercholesterolaemic subjects had either never been treated with lipid lowering therapy or therapy had been stopped at least two weeks before the study (n = 2). At the time of the study total plasma @entity165 levels (control: 4.6+/-0.3 vs hypercholesterolaemic: 8.3+/-0.6 mmol l(-1): P < 0.01) were significantly elevated in hypercholesterolaemic subjects when compared with controls. 4. Full concentration-response curves to the vasoconstrictor @entity1063 and the vasodilators @entity934 and @entity4757 were constructed. A single point concentration-response to @entity1854 (10 microM) was also obtained. Dilator responses were obtained in vessels pre-constricted with a submaximal concentration of @entity1063 . Vessels were then incubated for 30 min with either L- or @entity10834 (10 microM) and the concentration-response curves to the three dilator agonists repeated in the presence of the @entity535 . 5. Maximum relaxation responses to @entity934 (control vs hypercholesterolaemic: 83.3+/-6.1% vs 47.4+/-13.5%; P < 0.05), but not to @entity4757 or @entity1854 , were dampened in the hypercholesterolaemic group when compared with controls. 6. Neither incubation with @entity534 nor @entity10834 had any effect on maximum relaxation responses to @entity934 in either the control group (pre @entity534 vs plus @entity534 : 83.3+/-6.1 vs 82.3+/-5.5%, pre @entity10834 vs plus @entity10834 : 98.9+/-1.2 vs 98.2+/-1.1%) or the hypercholesterolaemic group (pre @entity534 vs plus @entity534 : 47.4+/-13.5 vs 55.3+/-14.3%, pre @entity10834 vs plus @entity10834 : 43.3+/-13.6 vs 65.4+/-12.3%). 7. When results from the two study groups were pooled, the strongest predictor of maximum relaxation obtained to @entity934 was apolipoprotein A1 (r = 0.67; P = 0.001). 8. In conclusion, relaxation responses mediated by the endothelium-dependent agonist @entity934 , but not by @entity4757 , are impaired in hypercholesterolaemic @entity1 . @entity534 did not improve the impaired relaxation responses to @entity934 . We suggest that impaired endothelium-dependent relaxation is specific to @entity934 and not to an abnormal @entity534 - @entity842 pathway in subcutaneous arteries excised from this study group.

Responses to endothelium-dependent agonists in subcutaneous arteries excised from hypercholesterolaemic XXXX .

@entity1 :: ('9606', 'Species') :: ['human', 'patients'] @entity10834 :: ('CHEBI:15816', 'Chemical') :: ['D-arginine'] @entity535 :: ('CHEBI:33704', 'Chemical') :: ['amino acid'] @entity1854 :: ('MESH:D009599', 'Chemical') :: ['sodium nitroprusside'] @entity534 :: ('CHEBI:16467', 'Chemical') :: ['L-arginine', 'L-Arginine'] @entity842 :: ('MESH:D009569', 'Chemical') :: ['nitric oxide'] @entity1063 :: ('MESH:D009638', 'Chemical') :: ['noradrenaline'] @entity4757 :: ('6863', 'Gene') :: ['substance P'] @entity165 :: ('MESH:D002784', 'Chemical') :: ['cholesterol'] @entity934 :: ('MESH:D000109', 'Chemical') :: ['acetylcholine']
@entity1 :: (9606,Species) :: ['men']
