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Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice
BACKGROUND: The effects of hypercholesterolemia on vasomotricity in apolipoprotein E-deficient (ApoE) mice, a murine model of spontaneous atherosclerosis, are still unclear. The studies were mostly performed in conductance vessels from male mice fed a high-fat diet. In the present study, we evaluate...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886002/ https://www.ncbi.nlm.nih.gov/pubmed/20482882 http://dx.doi.org/10.1186/1476-511X-9-51 |
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author | Cola, Maine S Gava, Agata L Meyrelles, Silvana S Vasquez, Elisardo C |
author_facet | Cola, Maine S Gava, Agata L Meyrelles, Silvana S Vasquez, Elisardo C |
author_sort | Cola, Maine S |
collection | PubMed |
description | BACKGROUND: The effects of hypercholesterolemia on vasomotricity in apolipoprotein E-deficient (ApoE) mice, a murine model of spontaneous atherosclerosis, are still unclear. The studies were mostly performed in conductance vessels from male mice fed a high-fat diet. In the present study, we evaluated the endothelial function of resistance vessels from normal C57BL/6 (C57) and hypercholesterolemic (ApoE) female mice in both normal and ovariectomized conditions. METHODS: Twenty week-old C57 and ApoE mice underwent ovariectomy or sham surgery and were studied 30 days later. The vascular reactivities to norepinephrine (NE, 10(-9 )to 2 × 10(-3 )mol/L), acetylcholine (ACh) and sodium nitroprusside (SNP) (10(-10 )to 10(-3 )mol/L) were evaluated in the isolated mesenteric arteriolar bed through dose-response curves. RESULTS: ACh-induced relaxation was significantly reduced (P < 0.05) in ApoE compared with C57 animals, as indicated by both the maximal response (37 ± 4% vs. 72 ± 1%) and the LogEC(50 )(-5.67 ± 0.18 vs. -6.23 ± 0.09 mol/L). Ovariectomy caused a significant impairment in ACh-induced relaxation in the C57 group (maximal response: 61 ± 4%) but did not worsen the deficient state of relaxation in ApoE animals (maximal response: 39 ± 5%). SNP-induced vasorelaxation and NE-induced vasoconstriction were similar in ApoE and C57 female mice. CONCLUSION: These data show an impairment of endothelial function in the resistance vessels of spontaneously atherosclerotic (ApoE-deficient) female mice compared with normal (C57) female mice. The endothelial dysfunction in hypercholesterolemic animals was so marked that ovariectomy, which impaired endothelial function in C57 mice, did not cause additional vascular damage in ApoE-deficient mice. |
format | Text |
id | pubmed-2886002 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-28860022010-06-16 Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice Cola, Maine S Gava, Agata L Meyrelles, Silvana S Vasquez, Elisardo C Lipids Health Dis Short Paper BACKGROUND: The effects of hypercholesterolemia on vasomotricity in apolipoprotein E-deficient (ApoE) mice, a murine model of spontaneous atherosclerosis, are still unclear. The studies were mostly performed in conductance vessels from male mice fed a high-fat diet. In the present study, we evaluated the endothelial function of resistance vessels from normal C57BL/6 (C57) and hypercholesterolemic (ApoE) female mice in both normal and ovariectomized conditions. METHODS: Twenty week-old C57 and ApoE mice underwent ovariectomy or sham surgery and were studied 30 days later. The vascular reactivities to norepinephrine (NE, 10(-9 )to 2 × 10(-3 )mol/L), acetylcholine (ACh) and sodium nitroprusside (SNP) (10(-10 )to 10(-3 )mol/L) were evaluated in the isolated mesenteric arteriolar bed through dose-response curves. RESULTS: ACh-induced relaxation was significantly reduced (P < 0.05) in ApoE compared with C57 animals, as indicated by both the maximal response (37 ± 4% vs. 72 ± 1%) and the LogEC(50 )(-5.67 ± 0.18 vs. -6.23 ± 0.09 mol/L). Ovariectomy caused a significant impairment in ACh-induced relaxation in the C57 group (maximal response: 61 ± 4%) but did not worsen the deficient state of relaxation in ApoE animals (maximal response: 39 ± 5%). SNP-induced vasorelaxation and NE-induced vasoconstriction were similar in ApoE and C57 female mice. CONCLUSION: These data show an impairment of endothelial function in the resistance vessels of spontaneously atherosclerotic (ApoE-deficient) female mice compared with normal (C57) female mice. The endothelial dysfunction in hypercholesterolemic animals was so marked that ovariectomy, which impaired endothelial function in C57 mice, did not cause additional vascular damage in ApoE-deficient mice. BioMed Central 2010-05-19 /pmc/articles/PMC2886002/ /pubmed/20482882 http://dx.doi.org/10.1186/1476-511X-9-51 Text en Copyright ©2010 Cola et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Short Paper Cola, Maine S Gava, Agata L Meyrelles, Silvana S Vasquez, Elisardo C Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice |
title | Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice |
title_full | Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice |
title_fullStr | Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice |
title_full_unstemmed | Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice |
title_short | Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice |
title_sort | endothelial dysfunction of resistance vessels in female apolipoprotein e-deficient mice |
topic | Short Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886002/ https://www.ncbi.nlm.nih.gov/pubmed/20482882 http://dx.doi.org/10.1186/1476-511X-9-51 |
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