Chronic stress improves NO- and Ca2+flux-dependent vascular function: a pharmacological study

• Autor(a) principal: Bruder-Nascimento, Thiago [UNESP]
• Data de Publicação: 2015
• Outros Autores: Campos, Dijon Henrique Salome [UNESP], Cicogna, Antonio Carlos [UNESP], Cordellini, Sandra [UNESP]
• Tipo de documento: Artigo
• Idioma: eng; por
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2015000300008&lng=en&nrm=iso&tlng=en; http://hdl.handle.net/11449/128573
• topic: Stress physiological / physiopatology; Hypertension; Nitric oxide / physiology; Rats; Vasoconstrictor agents / pharmacology; Estresse fisiológico / fisiopatologia; Hipertensão; Óxido nítrico / fisiologia; Ratos; Vasoconstritores / farmacologia

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, Ca2+ 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 Ca2+ 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 Ca2+-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.