Chronic social stress increases nitric oxide-dependent vasorelaxation in normotensive rats

Púzserová, Angelika; Bernátová, Iveta

doi:10.2478/v10102-010-0049-4

Cited by 11 publications

(6 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, exposing male rats or mice to social stress in the form of chronic crowding [72–74] or complex housing conditions [71] has been shown more often to enhance than to impair relaxant responses to ACh in precontracted arteries (including aorta but also femoral arteries). To our knowledge, there are no reports of enhanced endothelium-dependent relaxations in humans with depression or other affective disorders.…”

Section: Discussionmentioning

confidence: 99%

Chronic social isolation in the prairie vole induces endothelial dysfunction: implications for depression and cardiovascular disease

Peuler

Scotti

Phelps

et al. 2012

Physiology & Behavior

View full text Add to dashboard Cite

Humans with depression show impaired endothelium-dependent vasodilation, one recent demonstration of which was in the form of a reduced acetylcholine (ACh)-induced relaxation of adrenergically-precontracted small arteries biopsied from older depressed patients. Results from such uses of ACh in general have been validated as the most predictive marker of endothelium-related cardiovascular diseases. Accordingly, we examined vascular reactivity to ACh in the socially isolated prairie vole, a new animal model relevant to human depression and cardiovascular disease. Thoracic aortas were carefully dissected from female prairie voles after one month of social isolation (versus pairing with a sibling). Only aortas that contracted to the adrenergic agent phenylephrine (PE) and then relaxed to ACh were evaluated. Among those, ACh-induced relaxations were significantly reduced by social isolation (p<0.05), with maximum relaxation reaching only 30% (of PE-induced precontraction) compared to 47% in aortas from paired (control) animals. Experimental removal of the endothelium from an additional set of aortic tissues abolished all ACh relaxations including that difference. In these same tissues, maximally-effective concentrations of the nitric oxide-donor nitroprusside still completely relaxed all PE-induced precontraction of the endothelial-free smooth muscle, and to the same degree in tissues from isolated versus paired animals. Finally, in the absence of PE-induced precontraction ACh did not relax but rather contracted aortic tissues, and to a significantly greater extent in tissues from socially isolated animals if the endothelium was intact (p<0.05). Thus, social isolation in the prairie vole may 1) impair normal release of protective anti-atherosclerotic factors like nitric oxide from the vascular endothelium (without altering the inherent responsiveness of the vascular smooth muscle to such factors) and 2) cause the endothelium to release contracting factors. To our knowledge this is the first demonstration of this phenomenon in an animal model of depression induced solely by social isolation. These findings have implications for understanding mechanisms involved in depression and cardiovascular disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Chronic social isolation in the prairie vole induces endothelial dysfunction: implications for depression and cardiovascular disease

Peuler

Scotti

Phelps

et al. 2012

Physiology & Behavior

View full text Add to dashboard Cite

show abstract

“…In contrast, we observed elevated aortic NOS activity and improved endothelium-dependent relaxation, including its NO-dependent component, in the femoral artery of normotensive rats exposed to crowding (Púzserová et al 2006;Bernátová et al 2007b). Improved NO-dependent relaxation in crowded rats was observed in the femoral artery both in the presence and absence of AsA in working PSS, suggesting no significant influence of oxidative stress on elevated NO level in this artery (Puzserova and Bernatova 2010). Interestingly, the improvement of acetylcholine-induced relaxation in 1MA was seen only in the presence of AsA (Bernátová et al 2007b), while in this study, where AsA was removed, no considerable effect of stress was observed.…”

Section: Discussionmentioning

confidence: 49%

“…After the last acetylcholine concentration, the NO donor sodium nitroprusside (100 μmol/l) was added to the bath to check endothelium-independent NO vasodilator function. The NO-dependent component of endothelium-dependent relaxation was calculated as the difference between acetylcholine-induced relaxation before and after acute L-NAME pre-treatment and expressed as the area under the curve (AUC, arbitrary units) based on individual concentration-response curves (Puzserova and Bernatova 2010). In our preliminary experiments we ruled out tachyphylaxis (Hansen and Nedergaard 1999) in two consecutive concentration-response curves for acetylcholine in phenylephrine pre-contracted 1MA (data not shown).…”

Section: Experimental Protocol For Functional Studies Of the First Brmentioning

confidence: 99%

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

Púzserová

Török²,

Sotníková³

et al. 2012

gpb

Self Cite

View full text Add to dashboard Cite

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.

show abstract

“…It has recently been shown in animal models that depression-like symptoms are associated with changes in catecholamines homeostasis and endothelial dysfunction in resistance arteries. 76 , 77 , 123 These animal studies grant a unique opportunity to provide mechanistic understanding of cardiovascular abnormalities in association with depression symptoms. Moreover, these studies suggest a mechanism relevant for the unwanted circulatory effects of some antidepressants in depressive patients.…”

Section: Perspectivesmentioning

confidence: 99%

Role of Peripheral Vascular Resistance for the Association Between Major Depression and Cardiovascular Disease

Bouzinova

Wiborg

Aalkjær

et al. 2015

Journal of Cardiovascular Pharmacology

View full text Add to dashboard Cite

Abstract:Major depression and cardiovascular diseases are 2 of the most prevalent health problems in Western society, and an association between them is generally accepted. Although the specific mechanism behind this comorbidity remains to be elucidated, it is clear that it has a complex multifactorial character including a number of neuronal, humoral, immune, and circulatory pathways. Depression-associated cardiovascular abnormalities associate with cardiac dysfunctions and with changes in peripheral resistance. Although cardiac dysfunction in association with depression has been studied in detail, little attention was given to structural and functional changes in resistance arteries responsible for blood pressure control and tissue perfusion. This review discusses recent achievements in studies of depression-associated abnormalities in resistance arteries in humans and animal experimental models. The changes in arterial structure, contractile and relaxing functions associated with depression symptoms are discussed, and the role of these abnormalities for the pathology of major depression and cardiovascular diseases are suggested.

show abstract

Chronic social stress increases nitric oxide-dependent vasorelaxation in normotensive rats

Cited by 11 publications

References 30 publications

Chronic social isolation in the prairie vole induces endothelial dysfunction: implications for depression and cardiovascular disease

Chronic social isolation in the prairie vole induces endothelial dysfunction: implications for depression and cardiovascular disease

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

Role of Peripheral Vascular Resistance for the Association Between Major Depression and Cardiovascular Disease

Contact Info

Product

Resources

About