Evaluation of the brain and kidney renin-angiotensin system and oxidative stress in neonatal handled rats

2011 ◽  
Vol 54 (7) ◽  
pp. 706-713 ◽  
Author(s):  
Daniela L. Rodriguez ◽  
Fernanda C. de Mesquita ◽  
Débora Attolini ◽  
Bruna S. de Borba ◽  
Patrícia S. Scherer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain ◽  
And Oxidative Stress

Abstract 1375: Brain Renin Angiotensin Blockade Attenuates Cytokines and Oxidative Stress in the Paraventricular Nucleus of Hypothalamus and Decreases Sympathoexcitation in Heart Failure Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Ying Ma ◽  
Yu-Ming Kang* ◽  
Zhi-Ming Yang ◽  
Joseph Francis*
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Paraventricular Nucleus ◽  
Cross Talk ◽  
Renin Angiotensin System ◽  
Heart Weight ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain ◽  
And Oxidative Stress

Introduction: Neurohumoral mechanisms play an important role in the pathophysiology of congestive heart failure (HF). Recent studies suggest that the brain renin angiotensin system (RAS) plays an important role in regulating body fluids and sympathetic drive in HF. In addition, it has been shown that there is cross talk between cytokines and RAS in cardiovascular disease. In this study we determined whether blockade of brain RAS attenuate inflammatory cytokines and oxidative stress in HF rats. Methods and Results: Adult male Sprague-Dawley rats were implanted with intracerebroventricular (ICV) cannulae and subjected to coronary artery ligation to induce HF and confirmed by echocardiography. Rats were treated with an angiotensin type 1 receptors (AT1-R) antagonist losartan (LOS, 20 μg/hr, ICV) or vehicle (VEH) for 4 weeks. At the end of the study, left ventricular (LV) function was measured by echocardiography and rats were sacrificed, and brain and plasma samples were collected for measurements of cytokines and superoxide using immunohistochemistry, Western blot and real time RT-PCR. HF rats induced significant increases in Nuclear Factor-kappaB (NF-κB) p50-positive neurons and activated microglia in the paraventricular nucleus (PVN) of hypothalamus, and TNF-α, IL-1β, IL-6 and NF-κB p50 in hypothalamus when compared with sham rats. These animals also had increased staining for dihydroethidium (DHE) and plasma levels of norepinephrine (NE), an indirect indicator of sympathetic activity. In contrast, ICV treatment with LOS attenuated cytokine expression and oxidative stress in the PVN and hypothalamus when compared with VEH treated HF rats. ICV treatment with LOS also reduced plasma NE levels, and proinflammatory cytokine, heart weight to body weight ratio with decreased LV end-diastolic pressure. Conclusions : These findings suggest the cross talk between the cytokines and renin angiotensin system within the brain contribute to sympatho-excitation in HF.

scholarly journals Current aspects of the interactions between dementia, the brain renin-angiotensin system and oxidative stress

2015 ◽  
Vol 67 (3) ◽  
pp. 903-907 ◽  
Author(s):  
Dragomir Serban ◽  
Emil Anton ◽  
Roxana Chirita ◽  
Veronica Bild ◽  
Alin Ciobica ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Drug Use ◽  
Antihypertensive Drug ◽  
Renin Angiotensin System ◽  
Vascular Disorders ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Treatment And Prevention ◽  
The Brain ◽  
And Oxidative Stress

There is increased interest in the interactions between vascular disorders and Alzheimer?s disease (AD). While initially these interactions were explained by the fact that these are both very common disorders, particularly later in life, recently, the possibility that these deficiencies might actually coexist is increasingly being questioned. This review attempts to present modern aspects and current reports regarding the interactions between AD, the renin-angiotensin system (RAS) and hypertension, while also describing the relevance of antihypertensive drug use acting via the RAS in the treatment and prevention of AD, as well as the importance of oxidative stress, the alteration of the balance between antioxidants and pro-oxidants, in the interaction between AD and the RAS.

Aldosterone acts centrally to increase brain renin-angiotensin system activity and oxidative stress in normal rats

2008 ◽  
Vol 294 (2) ◽  
pp. H1067-H1074 ◽  
Author(s):  
Zhi-Hua Zhang ◽  
Yang Yu ◽  
Yu-Ming Kang ◽  
Shun-Guang Wei ◽  
Robert B. Felder
Keyword(s):  
Oxidative Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renin Angiotensin System ◽  
Nerve Activity ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Ru 28318 ◽  
The Brain ◽  
And Oxidative Stress

Aldosterone acts upon mineralocorticoid receptors in the brain to increase blood pressure and sympathetic nerve activity, but the mechanisms are still poorly understood. We hypothesized that aldosterone increases sympathetic nerve activity by upregulating the renin-angiotensin system (RAS) and oxidative stress in the brain, as it does in peripheral tissues. In Sprague-Dawley rats, aldosterone (Aldo) or vehicle (Veh) was infused for 1 wk via an intracerebroventricular (ICV) cannula, while RU-28318 (selective mineralocorticoid receptor antagonist), Tempol (superoxide dismutase mimetic), losartan [angiotensin II type 1 receptor (AT1R) antagonist], or Veh was infused simultaneously via a second ICV cannula. After 1 wk of ICV Aldo, plasma norepinephrine was increased and mean arterial pressure was slightly elevated, but heart rate was unchanged. These effects were ameliorated by ICV infusion of RU-28318, Tempol or losartan. Aldo increased expression of AT1R and angiotensin-converting enzyme (ACE) mRNA in hypothalamic tissue. RU-28318 minimized and Tempol prevented the increase in AT1R mRNA; RU-28318 prevented the increase in ACE mRNA. Losartan had no effect on AT1R or ACE mRNA. Immunohistochemistry revealed Aldo-induced increases in dihydroethidium staining (indicating oxidative stress) and Fra-like activity (indicating neuronal excitation) in neurons of the hypothalamic paraventricular nucleus (PVN). RU-28318 prevented the increases in superoxide and Fra-like activity in PVN; Tempol and losartan minimized these effects. Acute ICV infusions of sarthran (AT1R antagonist) or Tempol produced greater sympathoinhibition in Aldo-treated than in Veh-treated rats. Thus aldosterone upregulates key elements of brain RAS and induces oxidative stress in the hypothalamus. Aldosterone may increase sympathetic nerve activity by these mechanisms.

INHIBITION OF THE RENIN?ANGIOTENSIN SYSTEM ATTENUATES THE DEVELOPMENT OF LIVER FIBROSIS AND OXIDATIVE STRESS IN RATS

2007 ◽  
Vol 0 (0) ◽  
pp. 070928213402001-??? ◽  
Author(s):  
Ebtehal El-Demerdash ◽  
Omar M Abdel Salam ◽  
Seham A El-Batran ◽  
Heba MI Abdallah ◽  
Nermeen M Shaffie
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
And Oxidative Stress

scholarly journals Role of Renin-Angiotensin System and Oxidative Stress on Vascular Inflammation in Insulin Resistence Model

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
N. F. Renna ◽  
C. Lembo ◽  
E. Diez ◽  
R. M. Miatello
Keyword(s):  
Oxidative Stress ◽  
Experimental Model ◽  
Chronic Treatment ◽  
Vascular Tissue ◽  
Vascular Inflammation ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Creation ◽  
And Oxidative Stress

(1) This study aims to demonstrate the causal involvement of renin angiotensin system (RAS) and oxidative stress (OS) on vascular inflammation in an experimental model of metabolic syndrome (MS) achieved by fructose administration to spontaneously hypertensive rats (FFHR) during 12 weeks. (2) Chronic treatment with candesartan (C) (10 mg/kg per day for the last 6 weeks) or 4OH-Tempol (T) (10−3 mmol/L in drinking water for the last 6 weeks) reversed the increment in metabolic variables and systolic blood pressure. In addition, chronic C treatment reverted cardiovascular remodeling but not T. (3) Furthermore, chronic treatment with C was able to completely reverse the expression of NF-κB and VCAM-1, but T only reduced the expression. C reduced the expression of proatherogenic cytokines as CINC2, CINC3, VEGF, Leptin, TNF-alpha, and MCP-1 and also significantly reduced MIP-3, beta-NGF, and INF-gamma in vascular tissue in this experimental model. T was not able to substantially modify the expression of these cytokines. (4) The data suggest the involvement of RAS in the expression of inflammatory proteins at different vascular levels, allowing the creation of a microenvironment suitable for the creation, perpetuation, growth, and destabilization of vascular injury.

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