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 Ca2+ 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, Ca2+ 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 Ca2+ 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 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. (Arq Bras Cardiol. 2014; [online].ahead print,
PP.0-0)