ArticleArquivos brasileiros de cardiologia2015
Chronic stress improves NO- and Ca2+ flux-dependent vascular function: a pharmacological study.
Article in Arquivos brasileiros de cardiologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Effects of physical training on the metabolic profile of rats exposed to chronic restraint stress.Clinics (Sao Paulo, Brazil) · 2024Article
- Recent Progress of Chronic Stress in the Development of Atherosclerosis.Oxidative medicine and cellular longevity · 2022Review
- Myorelaxant Effect of theMolecules (Basel, Switzerland) · 2021Article
- Observational
- Emotional Stress and Cardiovascular Complications in Animal Models: A Review of the Influence of Stress Type.Frontiers in physiology · 2016Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStress is associated with cardiovascular diseases.
objectiveThis study aimed at assessing whether chronic stress induces vascular alterations, and whether these modulations are nitric oxide (NO) and Ca(2+) dependent.
methodsWistar 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.
resultsChronic 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.
conclusionOur 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.
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