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Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A Pharmacological Study
BACKGROUND: Stress is associated with cardiovascular diseases. OBJECTIVE: This study aimed at assessing whether chronic stress induces vascular alterations, and whether these modulations are nitric oxide (NO) and Ca2+ dependent. METHODS: Wistar rats, 30 days of age, were separated into 2 groups: con...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Sociedade Brasileira de Cardiologia
2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4386851/ https://www.ncbi.nlm.nih.gov/pubmed/25884770 http://dx.doi.org/10.5935/abc.20140207 |
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author | Bruder-Nascimento, Thiago Campos, Dijon Henrique Salome |
author_facet | Bruder-Nascimento, Thiago Campos, Dijon Henrique Salome |
author_sort | Bruder-Nascimento, Thiago |
collection | PubMed |
description | BACKGROUND: Stress is associated with cardiovascular diseases. OBJECTIVE: This study aimed at assessing whether chronic stress induces vascular alterations, and whether these modulations are nitric oxide (NO) and Ca2+ dependent. METHODS: Wistar rats, 30 days of age, were separated into 2 groups: control (C) and Stress (St). Chronic stress consisted of immobilization for 1 hour/day, 5 days/week, 15 weeks. Systolic blood pressure was assessed. Vascular studies on aortic rings were performed. Concentration-effect curves were built for noradrenaline, in the presence of L-NAME or prazosin, acetylcholine, sodium nitroprusside and KCl. In addition, Ca(2+) flux was also evaluated. RESULTS: Chronic stress induced hypertension, decreased the vascular response to KCl and to noradrenaline, and increased the vascular response to acetylcholine. L-NAME blunted the difference observed in noradrenaline curves. Furthermore, contractile response to Ca(2+) was decreased in the aorta of stressed rats. CONCLUSION: Our data suggest that the vascular response to chronic stress is an adaptation to its deleterious effects, such as hypertension. In addition, this adaptation is NO- and Ca(2+)-dependent. These data help to clarify the contribution of stress to cardiovascular abnormalities. However, further studies are necessary to better elucidate the mechanisms involved in the cardiovascular dysfunction associated with stressors. (Arq Bras Cardiol. 2014; [online].ahead print, PP.0-0) |
format | Online Article Text |
id | pubmed-4386851 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Sociedade Brasileira de Cardiologia |
record_format | MEDLINE/PubMed |
spelling | pubmed-43868512015-04-07 Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A Pharmacological Study Bruder-Nascimento, Thiago Campos, Dijon Henrique Salome Arq Bras Cardiol Original Articles BACKGROUND: Stress is associated with cardiovascular diseases. OBJECTIVE: This study aimed at assessing whether chronic stress induces vascular alterations, and whether these modulations are nitric oxide (NO) and Ca2+ dependent. METHODS: Wistar rats, 30 days of age, were separated into 2 groups: control (C) and Stress (St). Chronic stress consisted of immobilization for 1 hour/day, 5 days/week, 15 weeks. Systolic blood pressure was assessed. Vascular studies on aortic rings were performed. Concentration-effect curves were built for noradrenaline, in the presence of L-NAME or prazosin, acetylcholine, sodium nitroprusside and KCl. In addition, Ca(2+) flux was also evaluated. RESULTS: Chronic stress induced hypertension, decreased the vascular response to KCl and to noradrenaline, and increased the vascular response to acetylcholine. L-NAME blunted the difference observed in noradrenaline curves. Furthermore, contractile response to Ca(2+) was decreased in the aorta of stressed rats. CONCLUSION: Our data suggest that the vascular response to chronic stress is an adaptation to its deleterious effects, such as hypertension. In addition, this adaptation is NO- and Ca(2+)-dependent. These data help to clarify the contribution of stress to cardiovascular abnormalities. However, further studies are necessary to better elucidate the mechanisms involved in the cardiovascular dysfunction associated with stressors. (Arq Bras Cardiol. 2014; [online].ahead print, PP.0-0) Sociedade Brasileira de Cardiologia 2015-03 /pmc/articles/PMC4386851/ /pubmed/25884770 http://dx.doi.org/10.5935/abc.20140207 Text en http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Bruder-Nascimento, Thiago Campos, Dijon Henrique Salome Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A Pharmacological Study |
title | Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A
Pharmacological Study |
title_full | Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A
Pharmacological Study |
title_fullStr | Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A
Pharmacological Study |
title_full_unstemmed | Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A
Pharmacological Study |
title_short | Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A
Pharmacological Study |
title_sort | chronic stress improves no- and ca2+ flux-dependent vascular function: a
pharmacological study |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4386851/ https://www.ncbi.nlm.nih.gov/pubmed/25884770 http://dx.doi.org/10.5935/abc.20140207 |
work_keys_str_mv | AT brudernascimentothiago chronicstressimprovesnoandca2fluxdependentvascularfunctionapharmacologicalstudy AT camposdijonhenriquesalome chronicstressimprovesnoandca2fluxdependentvascularfunctionapharmacologicalstudy |