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

• Published in: Arquivos brasileiros de cardiologia Vol. 104; no. 3; pp. 226 - 233
• Main Authors: Bruder-Nascimento, Thiago, Campos, Dijon Henrique Salome, Cicogna, Antônio Carlose, Cordellini, Sandra
• Format: Journal Article
• Language: English; Portuguese
• Published: Brazil Sociedade Brasileira de Cardiologia 01.03.2015; Sociedade Brasileira de Cardiologia - SBC; Sociedade Brasileira de Cardiologia (SBC)
• Subjects: Animals; Aorta, Thoracic - metabolism; Aorta, Thoracic - physiopathology; Blood Pressure - physiology; Calcium - metabolism; Calcium Chloride - analysis; CARDIAC & CARDIOVASCULAR SYSTEMS; Cardiovascular Diseases - etiology; Cardiovascular Diseases - metabolism; Cardiovascular Diseases - physiopathology; Corticosterone - blood; Endothelium, Vascular - metabolism; Endothelium, Vascular - physiopathology; Estresse Fisiológico / fisiopatologia; Hipertensão; Male; NG-Nitroarginine Methyl Ester - analysis; Nitric Oxide - metabolism; Norepinephrine - analysis; Original; Potassium Chloride - analysis; Ratos; Rats, Wistar; Reference Values; Stress, Psychological - complications; Stress, Psychological - metabolism; Stress, Psychological - physiopathology; Vasoconstritores / farmacologia; Óxido Nítrico / fisiologia; Hypertension; Stress, Physiological / physiopatology; Nitric Oxide / physiology; Óxido Nítrico / fisiologia; Vasoconstritores / farmacologia; Rats; Ratos; Estresse Fisiológico / fisiopatologia; Hipertensão; Vasoconstrictor Agents / pharmacology
• ISSN: 0066-782X; 1678-4170; 1678-4170
• DOI: 10.5935/abc.20140207

Stress is associated with cardiovascular diseases. This study aimed at assessing whether chronic stress induces vascular alterations, and whether these modulations are nitric oxide (NO) and Ca(2+) dependent. 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. 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. 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.