Reactivity of the mesenteric bed arteries of normotensive rats exposed to chronic social stress

Abstract

The aim of this study was to investigate the effects of chronic social stress on endothelium-dependent relaxation in the superior mesenteric artery (SMA) and its first branches (1MA) as well as on neurogenic contractions of SMA in adult, male Wistar-Kyoto (WKY) rats. Mesenteric arteries were isolated from control (living space: 480 cm(2)/rat) or stressed rats exposed to 8-week-lasting crowding stress (living space: 200 cm(2)/rat). Blood pressure (BP) and heart rate, determined by tail-cuff plethysmography, were not affected by crowding. Stress increased neurogenic contractions of SMA elicited by electrical stimulation of perivascular nerves and significantly elevated vasoconstriction induced by exogenous noradrenaline in SMA, without modulation of its endothelial function. In 1MA, nitric oxide (NO)-dependent component of endothelium-dependent relaxation to acetylcholine was investigated. In 1MA, stress failed to affect noradrenaline- and phenylephrine-induced vasoconstriction, total acetylcholine-induced relaxation as well as its NO-dependent and NO-independent components. Moreover, endothelium-independent sodium nitroprusside-induced relaxations of 1MA from the stressed rats did not differ from those of controls. In conclusion, chronic stress produced by crowding failed to induce an increase of BP, presumably because endothelial function of SMA and vascular function of small mesenteric arteries, which are rather important in BP regulation, remained preserved.

Chronic stress impacts the cardiovascular system: animal models and clinical outcomes

“…In an animal study conducted by Isingrini et al (153), unpredictable chronic mild stress induced hormonal and depression-related physical behaviors along with decreased endothelium-dependent vasorelaxation. In this study, stress did not affect phenylephrine-induced vasoconstriction, whereas Puzserova et al (268) reported increased contractile responses to both electrical stimulation of perivascular nerves and exogenous norepinephrine without any discernible changes in nitric oxide (NO)-dependent vasorelaxation. Results from another experiment suggest that chronic mild stress increased phenylephrine-induced vasoconstriction in intact aortic ring segments, yet failed to show such effects in N G -nitro-L-arginine methyl ester-incubated or endothelium-denuded rings.…”

Comorbidity Factors and Brain Mechanisms Linking Chronic Stress and Systemic Illness

“…Recent human and animal studies have further demonstrated that stress can also lead to the development of vascular dysfunction resulting in a predisposition to CVD [ 154 – 157 ]. In addition, both acute and chronic stressors have been shown to impair vascular reactivity.…”

“…In addition, both acute and chronic stressors have been shown to impair vascular reactivity. Although the exact mechanism and effect seem to be dependent on the type of the stressor and/or the model, there is evidence to suggest that reduced vascular dilation and enhanced constriction may play an important role [ 156 , 157 ]. In humans, acute psychological stress reduces the magnitude of flow-mediated dilation of the brachial artery, a measure of the reactivity of the peripheral vasculature that is thought to be the result of altered nitric oxide handling [ 154 ].…”

Lisinopril reverses behavioural alterations in spontaneously hypertensive rats

“…Experimental cardiovascular pathologies are associated with different neuropsychiatric symptoms, while on the contrary, various mental disorders may support the progression of cardiovascular, neurohumoral or metabolic disorders (Pechanova et al 2006;Bernatova et al 2010;Puzserova et al 2012;Aziriova et al 2016;Olexova et al 2016;Pokusa et al 2016;Senko et al 2017;Repova et al 2018). In a clinical setting, patients with cardiac diseases suffer from post-traumatic stress disorder (Vilchinsky et al 2017), yet mental disorders not only impair their adherence to therapeutic management (Gentil et al 2017); they can also contribute to the progres-sion of cardiovascular diseases (Shields and Slavich 2017).…”