Acute restraint stress increases carotid reactivity in type-I diabetic rats by enhancing Nox4/NADPH oxidase functionality

Chronic restraint stress increases angiotensin II potency in the rat carotid: role of cyclooxygenases and reactive oxygen species

“…Rats from the stressed group were exposed to 3‐h restraint stress for 5 days. The restraint stress consisted in putting the rat into plastic tubes of 6.5 cm in diameter and adjustable length in 20–23 cm, with lateral holes to breathe . The functional and biochemical assays in isolated carotid rings were performed on day 5.…”

“…Corticosterone measurement by radioimmunoassays in serum samples, as previously described, was applied to validate the stress model (Table ). As previously validated in our laboratory, the model of 3‐h‐lasting restraint stress/day elicits an increase in rat corticosterone levels .…”

“…Corticosterone measurement by radioimmunoassays in serum samples, as previously described, was applied to validate the stress model (Table ). As previously validated in our laboratory, the model of 3‐h‐lasting restraint stress/day elicits an increase in rat corticosterone levels . At the 5th day of restraint stress, the rats develop an adaptation to the stressful condition and their serum corticosterone levels return to the control levels, which characterizes a chronic stress model .…”

“…Acute restraint stress exacerbates the vascular complications induced by type I diabetes in rat carotid by evoking a local angiotensinergic contractile hyperreactivity resulting from the activation of COXdependent proinflammatory pathways. [26] However, the exposure to acute restraint stress was not able to elicit significant changes in carotid responsiveness to angiotensinergic stimuli or in the local redox-proinflammatory signalling in normoglycaemic rats. [26] Based on the findings described above, we hypothesized that the exposure to chronic restraint stress may alter AngII-induced contraction in rat carotid by mechanisms associated with increased generation of ROS, COX-derived metabolites and activation of Akt signalling.…”

“…However, the participation of COX on AngII‐induced vascular contraction after chronic restraint stress exposure is not completely known. Acute restraint stress exacerbates the vascular complications induced by type I diabetes in rat carotid by evoking a local angiotensinergic contractile hyperreactivity resulting from the activation of COX‐dependent proinflammatory pathways . However, the exposure to acute restraint stress was not able to elicit significant changes in carotid responsiveness to angiotensinergic stimuli or in the local redox‐proinflammatory signalling in normoglycaemic rats …”