Genotype-Related Effect of Crowding Stress on Blood Pressure and Vascular Function in Young Female Rats

Slezák, Peter; Púzserová, Angelika; Bališ, Peter; Sestakova, Natalia; Majzúnová, Miroslava; Dovinová, Ima; Kluknavsky, Michal; Bernátová, Iveta

doi:10.1155/2014/413629

Cited by 18 publications

(31 citation statements)

References 51 publications

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“…However, despite higher BP and vascular ROS production, we did not observe ED in these rats as reduced NO-dependent relaxation was fully compensated be elevated NO-independent relaxation [98]. Thus, our findings in young BHR rats are not supportive of the idea that ED precedes hypertension in this particular model of hypertension.…”

Section: Endothelial Dysfunction In Experimental Hypertensioncontrasting

confidence: 61%

“…Interestingly, at all time points investigated, we always found elevated vascular NO production in the aorta of stress-exposed WKY [98, 141–143]. Despite the consistency in these findings, the effect on vascular function was variable.…”

Section: Endothelial Dysfunction In Experimental Hypertensionmentioning

confidence: 72%

“…Elevated ROS production was observed in the aorta of young BHR and SHR [98] as well as in adult SHR [45, 101]. …”

Section: Endothelial Dysfunction In Experimental Hypertensionmentioning

confidence: 99%

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Endothelial Dysfunction in Experimental Models of Arterial Hypertension: Cause or Consequence?

Bernátová

2014

BioMed Research International

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Hypertension is a risk factor for other cardiovascular diseases and endothelial dysfunction was found in humans as well as in various commonly employed animal experimental models of arterial hypertension. Data from the literature indicate that, in general, endothelial dysfunction would not be the cause of experimental hypertension and may rather be secondary, that is, resulting from high blood pressure (BP). The initial mechanism of endothelial dysfunction itself may be associated with a lack of endothelium-derived relaxing factors (mainly nitric oxide) and/or accentuation of various endothelium-derived constricting factors. The involvement and role of endothelium-derived factors in the development of endothelial dysfunction in individual experimental models of hypertension may vary, depending on the triggering stimulus, strain, age, and vascular bed investigated. This brief review was focused on the participation of endothelial dysfunction, individual endothelium-derived factors, and their mechanisms of action in the development of high BP in the most frequently used rodent experimental models of arterial hypertension, including nitric oxide deficient models, spontaneous (pre)hypertension, stress-induced hypertension, and selected pharmacological and diet-induced models.

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Section: Endothelial Dysfunction In Experimental Hypertensioncontrasting

confidence: 61%

Section: Endothelial Dysfunction In Experimental Hypertensionmentioning

confidence: 72%

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Endothelial Dysfunction in Experimental Models of Arterial Hypertension: Cause or Consequence?

Bernátová

2014

BioMed Research International

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“…The production of superoxide (O 2 ∙− ) was measured in tissue samples of the LHV and thoracic aorta (15–20 mg) by lucigenin-enhanced chemiluminescence (50 μ mol/L) using a TriCarb 2910TR liquid scintillation analyser (Perkin Elmer), as described previously [37]. The results are expressed as counts per minute per milligram of tissue (cpm/mg).…”

Section: Methodsmentioning

confidence: 99%

(−)‐Epicatechin Prevents Blood Pressure Increase and Reduces Locomotor Hyperactivity in Young Spontaneously Hypertensive Rats

Kluknavsky

Bališ

Púzserová

et al. 2016

Oxidative Medicine and Cellular Longevity

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This study investigated the effects of subchronic (−)-epicatechin (Epi) treatment on locomotor activity and hypertension development in young spontaneously hypertensive rats (SHR). Epi was administered in drinking water (100 mg/kg/day) for 2 weeks. Epi significantly prevented the development of hypertension (138 ± 2 versus 169 ± 5 mmHg, p < 0.001) and reduced total distance traveled in the open-field test (22 ± 2 versus 35 ± 4 m, p < 0.01). In blood, Epi significantly enhanced erythrocyte deformability, increased total antioxidant capacity, and decreased nitrotyrosine concentration. In the aorta, Epi significantly increased nitric oxide (NO) synthase (NOS) activity and elevated the NO-dependent vasorelaxation. In the left heart ventricle, Epi increased NOS activity without altering gene expressions of nNOS, iNOS, and eNOS. Moreover, Epi reduced superoxide production in the left heart ventricle and the aorta. In the brain, Epi increased nNOS gene expression (in the brainstem and cerebellum) and eNOS expression (in the cerebellum) but had no effect on overall NOS activity. In conclusion, Epi prevented the development of hypertension and reduced locomotor hyperactivity in young SHR. These effects resulted from improved cardiovascular NO bioavailability concurrently with increased erythrocyte deformability, without changes in NO production in the brain.

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“…In our study, we used a model of social stress produced by the crowding that results from reduced living space (Slezak et al, 2014). This model seems to be more relevant to the human condition (D’Atri et al, 1981; Fleming et al, 1987) than other experimental models of chronic stress, as it “typically evokes social stress reactions with prominent psychosocial components, mimicking emotional state alterations” (Bugajski, 1999).…”

Section: Introductionmentioning

confidence: 99%

Chronic Stress Produces Persistent Increases in Plasma Corticosterone, Reductions in Brain and Cardiac Nitric Oxide Production, and Delayed Alterations in Endothelial Function in Young Prehypertensive Rats

et al. 2018

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This study was designed to investigate whether oxidative stress, nitric oxide (NO) deficiency and/or endothelial dysfunction (ED) are present in young borderline hypertensive rats (BHR) and whether these pathologies can be causally involved in the initiation of blood pressure (BP) increases. Additionally, we tested the hypothesis that crowding stress, experienced during the peripubertal period, may produce persistent or delayed disorders in corticosterone release, NO synthesis, oxidative status and/or endothelial function that could accelerate BP increases. To test these hypotheses, 5-week-old male BHR and normotensive Wistar-Kyoto rats (WKY) were either kept in control conditions (for 2 and 4 weeks, respectively) or exposed to social stress produced by crowding for 2 weeks (stress). After cessation of crowding, a group of rats of each phenotype was kept in control conditions for the next 2 weeks (post-stress). Systolic BP of 5-week-old BHR was significantly increased vs. age-matched WKY (127 ± 3 vs. 104 ± 3 mmHg, p < 0.01) and remained significantly higher throughout the course of the experiment. Despite elevated BP, no signs of oxidative damage to plasma lipids, NO deficiency or ED were observed in control BHR vs. age-matched WKY. Crowding stress elevated plasma corticosterone and accelerated BP increases only in BHR; these effects persisted 2 weeks post-stress. Crowding failed to induce oxidative damage to plasma lipids in either phenotype, but it produced persistent decreases in NO production in the hypothalamus and brainstem of both strains of rats, as well as in the hearts of BHR. In contrast, crowding failed to reduce NO production in the aortae or acetylcholine-induced relaxations of the femoral arteries in both strains investigated. However, significantly reduced aortic NO production was observed in BHR 2 weeks post-stress vs. age-matched controls, which was in agreement with reduced NO-dependent components of vasorelaxation. In conclusion, this study’s data showed that oxidative stress, NO deficiency and ED are not causally involved in initiation of blood pressure increase in BHR. However, exposure to stressful environments produced persistent increases in plasma corticosterone and reductions of brain and cardiac NO production followed by a delayed decrease in the NO-dependent component of endothelium-dependent relaxation—changes that collectively accelerated BP increases only in BHR.

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Genotype-Related Effect of Crowding Stress on Blood Pressure and Vascular Function in Young Female Rats

Cited by 18 publications

References 51 publications

Endothelial Dysfunction in Experimental Models of Arterial Hypertension: Cause or Consequence?

Endothelial Dysfunction in Experimental Models of Arterial Hypertension: Cause or Consequence?

(−)‐Epicatechin Prevents Blood Pressure Increase and Reduces Locomotor Hyperactivity in Young Spontaneously Hypertensive Rats

Chronic Stress Produces Persistent Increases in Plasma Corticosterone, Reductions in Brain and Cardiac Nitric Oxide Production, and Delayed Alterations in Endothelial Function in Young Prehypertensive Rats

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