Strain-dependent differences of restraint stress-induced hypertension in WKY and SHR

Grundt, Alexander; Grundt, Christina; Gorbey, Stefan; Thomas, Martin Alexander

doi:10.1016/j.physbeh.2009.02.029

Cited by 46 publications

(26 citation statements)

References 18 publications

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“…The strain difference observed during exercise could be related to greater tolerance to exercise-induced stress secondary to the higher basal BP in SHRs. The reason for the difference observed in restraining is not clear, although it could be related to the greater response in SHRs to the stress induced by restraining and from BP measurement by the tail cuff method [Grundt et al 2009 ]. It will be very exciting to follow up the exercise study using another cardiovascular disease model such as spontaneous hypertensive heart failure (congenic) or the coronary artery ligation myoinfarct model to explore if they also have an altered response to exercise.…”

Section: Discussionmentioning

confidence: 99%

Effect of acute exercise on cardiovascular hemodynamic and red blood cell concentrations of purine nucleotides in hypertensive compared with normotensives rats

Yeung

Dauphinee

Marcoux

2013

Therapeutic Advances in Cardiovascular Disease

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Section: Discussionmentioning

confidence: 99%

Effect of acute exercise on cardiovascular hemodynamic and red blood cell concentrations of purine nucleotides in hypertensive compared with normotensives rats

Yeung

Dauphinee

Marcoux

2013

Therapeutic Advances in Cardiovascular Disease

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“…To measure blood pressure continuously without disturbing the animal's natural behavior we used a previously reported protocol [34]. After implantation of the devices, STZdiabetic rats were randomly administrated i.p.…”

Section: Telemetric Blood Pressure Measurementmentioning

confidence: 99%

Long-term Treatment with Suberythropoietic Epo is Vaso- and Neuroprotective in Experimental Diabetic Retinopathy

Wang

Gorbey

Pfister

et al. 2011

Cell Physiol Biochem

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Background/Aims: Diabetic retinopathy is characterized by pericyte loss and vasoregression both in the clinic and in animal models. A mild neurodegeneration with loss of ganglion cells is also described in the diabetic retina. Like VEGF-A, Epo is angioprotective and, in high doses, neuroprotective, however, without affecting vessel permeability. This study was to investigate the effect of a long-term suberythropoietic dose of Epo on vascular damage and neurodegeneration in a rat model of diabetic retinopathy. Methods: We administered Epo 3x256 IU/kg body weight/week to streptozotocin-diabetic Wistar rats for up to 6 months. Leukostasis was analyzed by quantitation of CD45 positive cells adherent to the retinal microvasculature. VEGF-A levels were assessed by Elisa at 3 months of treatment. Vasoregression was quantified in retinal digest preparations after 6 months of Epo treatment.Neurodegeneration was analyzed from PAS stained retinal paraffin preparations. Results: Leukostasis was unaffected by treatment with Epo which significantly inhibited the loss of pericyte and the formation of acellular capillaries. Neurodegeneration in the diabetic retina was significantly reduced by Epo treatment. Increased VEGF-A levels in the diabetic retina were normalized by Epo treatment. Conclusions: Suberythropoietic Epo is effective to protect microvascular and neuronal damage in the experimental diabetic retina.

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“…Moreover, PVN AT 1 R expression is increased in SHRs and in normotensive rats following repeated restraint and 24-h isolation stress (51), and systemic administration of an AT 1 R antagonist blunts the sympathoadrenal response to stress in SHRs (25). Results from this study suggest that the lack of MIF negative feedback on ANG II-mediated neuronal activation within the PVN could contribute to enhanced stress sensitivity in SHRs.…”

Section: Discussionmentioning

confidence: 78%

Novel mechanism within the paraventricular nucleus reduces both blood pressure and hypothalamic pituitary-adrenal axis responses to acute stress

Erdös

Clifton

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Erdos B, Clifton RR, Liu M, Li H, McCowan ML, Sumners C, Scheuer DA. Novel mechanism within the paraventricular nucleus reduces both blood pressure and hypothalamic pituitary-adrenal axis responses to acute stress. Am J Physiol Heart Circ Physiol 309: H634-H645, 2015. First published June 12, 2015 doi:10.1152/ajpheart.00207.2015.-Macrophage migration inhibitory factor (MIF) counteracts pressor effects of angiotensin II (ANG II) in the paraventricular nucleus of the hypothalamus (PVN) in normotensive rats, but this mechanism is absent in spontaneously hypertensive rats (SHRs) due to a lack of MIF in PVN neurons. Since endogenous ANG II in the PVN modulates stress reactivity, we tested the hypothesis that replacement of MIF in PVN neurons would reduce baseline blood pressure and inhibit stressinduced increases in blood pressure and plasma corticosterone in adult male SHRs. Radiotelemetry transmitters were implanted to measure blood pressure, and then an adeno-associated viral vector expressing either enhanced green fluorescent protein (GFP) or MIF was injected bilaterally into the PVN. Cardiovascular responses to a 15-min water stress (1-cm deep, 25°C) and a 60-min restraint stress were evaluated 3-4 wk later. MIF treatment in the PVN attenuated average restraintinduced increases in blood pressure (37.4 Ϯ 2.0 and 27.6 Ϯ 3.5 mmHg in GFP and MIF groups, respectively, P Ͻ 0.05) and corticosterone (42 Ϯ 2 and 36 Ϯ 3 g/dl in GFP and MIF groups, respectively, P Ͻ 0.05). MIF treatment in the PVN also reduced stress-induced elevations in the number of c-Fos-positive cells in the rostral ventrolateral medulla (71 Ϯ 5 in GFP and 47 Ϯ 5 in MIF SHRs, P Ͻ 0.01) and corticotropin-releasing factor mRNA expression in the PVN. However, MIF had no significant effects on the cardiovascular responses to water stress in SHRs or to either stress in Sprague-Dawley rats. Therefore, viral vector-mediated restoration of MIF in PVN neurons of SHRs attenuates blood pressure and hypothalamic pituitary adrenal axis responses to stress. psychological stress; blood pressure; brain; angiotensin ii; hypertension NEW & NOTEWORTHY Exaggerated activation of the sympathetic nervous system and/or the hypothalamic-pituitary-adrenal (HPA) axis increases cardiovascular disease risk. The present study demonstrates that macrophage migration inhibitory factor (MIF) in paraventricular nucleus (PVN) neurons is a novel mechanism mediating attenuation of both the sympathetic and HPA axis responses to acute stress.SEVERAL LINES OF EVIDENCE suggest that the amplitude of blood pressure increases in response to psychological or physical stressors in young and middle-aged normotensive adults elevates the risk of developing hypertension and other cardiovascular diseases such as coronary artery disease, myocardial ischemia, and stroke later in their life (8,20,39,41,42,44,50,60). Larger variations in blood pressure in response to repeated everyday stressors may lead to accelerated damage of the kidneys and vasculature. Altered central mechanisms that mediate augmented...

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Strain-dependent differences of restraint stress-induced hypertension in WKY and SHR

Cited by 46 publications

References 18 publications

Effect of acute exercise on cardiovascular hemodynamic and red blood cell concentrations of purine nucleotides in hypertensive compared with normotensives rats

Effect of acute exercise on cardiovascular hemodynamic and red blood cell concentrations of purine nucleotides in hypertensive compared with normotensives rats

Long-term Treatment with Suberythropoietic Epo is Vaso- and Neuroprotective in Experimental Diabetic Retinopathy

Novel mechanism within the paraventricular nucleus reduces both blood pressure and hypothalamic pituitary-adrenal axis responses to acute stress

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