Renin-angiotensin-aldosterone system-mediated redox effects in chronic kidney disease

Nistala, Ravi; Wei, Yongzhong; Sowers, James R.; Whaley‐Connell, Adam

doi:10.1016/j.trsl.2008.12.008

Cited by 34 publications

(24 citation statements)

References 102 publications

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“…Aldosterone regulates electrolyte, fluid balance and BP homoeostasis (Connell & Davies, 2005). It also mediates maladaptive tissue remodelling throughout the CVS and central nervous system (CNS), thereby, worsening the HTN (Nistala et al, 2009;Zannad et al, 2009;Aoki et al, 2010;Briet & Schiffrin, 2010;De-An et al, 2010;Whaley-Connell et al, 2010;Lymperopoulos et al, 2011). Therefore, a reduction in its plasma levels is advantageous to the animal.…”

Section: Plasma Aldosterone Levelsmentioning

confidence: 99%

Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats

Raji

Mugabo

Obikeze

2012

Journal of Ethnopharmacology

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Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats I. A. RAJITulbaghia violacea Harv. (Alliaceae) is a small bulbous herb which belongs to the family, Alliaceae, most commonly associated with onions and garlic. In South Africa (SA), this herb has been traditionally used in the treatment of various ailments, including fever, colds, asthma, paralysis, hypertension (HTN) and stomach problems. The aim of this study was to evaluate the effect of methanol leaf extracts (MLE) of T. violacea on the blood pressure (BP) and heart rate (HR) in anaesthetized male spontaneously hypertensive rats; and to find out the mechanism(s) by which it acts.The MLE of T. violacea (5 -150 mg/kg), angiotensin I (ang I, 3.1 -100 µg/kg), captopril (10 mg/kg), angiotensin II (ang II, 3.1 -50 µg/kg), losartan (30 mg/kg), phenylephrine T. violacea (60 mg/kg) and captopril (10 mg/kg) were injected intraperitoneally into iii some SHR for 21 days to investigate the chronic effect of these agents on plasma levels of aldosterone. The mean change, the mean of the individual percentage changes and the percentage difference (in mean) observed with each intervention was calculated and statistically analyzed using the Student's t test for significant difference (p < 0.05). The Microsoft Excel software was used for statistical analysis.T. violacea significantly (p < 0.05) reduced the systolic, diastolic, and mean arterial BP;and HR dose-dependently. In a dose-dependent manner, ang I, ang II, phenylephrine significantly (p < 0.05) increased the BP, while propranolol, muscarine and atropine reduced the BP. The increases in BP due to dobutamine were not dose-dependent. In a dose dependent manner, phenylephrine and propranolol reduced the HR, while dobutamine increased the HR. The effect of ang I, ang II, muscarine and atropine on HR were not dose-dependent; with both increases as well as decreases observed with ang I, and II and atropine, while decreases were seen with muscarine. Captopril produced significant (p < 0.05) reduction in BP which were not associated with any change in HR.The co-infusion of ang I with the MLE produced significant (p < 0.05) reduction in BP, which were not associated with significant changes in HR. The co-infusion of ang II with the MLE did not produce any significant changes in BP or HR when compared to the infusion of the standard drug alone. The co-infusion of phenylephrine with the MLE did

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Section: Plasma Aldosterone Levelsmentioning

confidence: 99%

Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats

Raji

Mugabo

Obikeze

2012

Journal of Ethnopharmacology

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“…Comprehensive reviews on the generation and actions of ROS in vascular and cardiac systems have been published recently (88,104,192,193,199,203,204,242,255,317,319). These publications have emphasized the contribution of pro-and antioxidant enzymes, the signaling pathways involved, and the approaches for prevention and treatment of hypertension with the use of antioxidants drugs.…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress in Hypertension: Role of the Kidney

Araújo

Wilcox

2014

Antioxidants & Redox Signaling

163

131

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Significance: Renal oxidative stress can be a cause, a consequence, or more often a potentiating factor for hypertension. Increased reactive oxygen species (ROS) in the kidney have been reported in multiple models of hypertension and related to renal vasoconstriction and alterations of renal function. Nicotinamide adenine dinucleotide phosphate oxidase is the central source of ROS in the hypertensive kidney, but a defective antioxidant system also can contribute. Recent Advances: Superoxide has been identified as the principal ROS implicated for vascular and tubular dysfunction, but hydrogen peroxide (H 2 O 2 ) has been implicated in diminishing preglomerular vascular reactivity, and promoting medullary blood flow and pressure natriuresis in hypertensive animals. Critical Issues and Future Directions: Increased renal ROS have been implicated in renal vasoconstriction, renin release, activation of renal afferent nerves, augmented contraction, and myogenic responses of afferent arterioles, enhanced tubuloglomerular feedback, dysfunction of glomerular cells, and proteinuria. Inhibition of ROS with antioxidants, superoxide dismutase mimetics, or blockers of the reninangiotensin-aldosterone system or genetic deletion of one of the components of the signaling cascade often attenuates or delays the onset of hypertension and preserves the renal structure and function. Novel approaches are required to dampen the renal oxidative stress pathways to reduced O 2 -rather than H 2 O 2 selectivity and/or to enhance the endogenous antioxidant pathways to susceptible subjects to prevent the development and renaldamaging effects of hypertension. Antioxid. Redox Signal. 20, 74-101.

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“…ROS production in vessels, as well as other organs, including the heart, kidneys and brain, likely participate in blood pressure regulation. [30][31][32] This review will focus on ROS, the vascular system and hypertension, specifically relating to the clinical significance. All vascular cell types produce ROS, including endothelial, smooth muscle, adventitial fibroblasts and perivascular adipocytes, and can be formed by many enzymes, including xanthine oxidoreductase, uncoupled nitric oxide synthase, mitochondrial respiratory enzymes and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase [37][38][39][40][41][42][43][44] (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

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Increased vascular production of reactive oxygen species (ROS; termed oxidative stress) has been implicated in various chronic diseases, including hypertension. Oxidative stress is both a cause and a consequence of hypertension. Although oxidative injury may not be the sole etiology, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors. Oxidative stress is a multisystem phenomenon in hypertension and involves the heart, kidneys, nervous system, vessels and possibly the immune system. Compelling experimental and clinical evidence indicates the importance of the vasculature in the pathophysiology of hypertension and as such much emphasis has been placed on the (patho)biology of ROS in the vascular system. A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4. Nox-derived ROS is important in regulating endothelial function and vascular tone. Oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in hypertension. Despite a plethora of data implicating oxidative stress as a causative factor in experimental hypertension, findings in human hypertension are less conclusive. This review highlights the importance of ROS in vascular biology and focuses on the potential role of oxidative stress in human hypertension.

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Renin-angiotensin-aldosterone system-mediated redox effects in chronic kidney disease

Cited by 34 publications

References 102 publications

Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats

Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats

Oxidative Stress in Hypertension: Role of the Kidney

Reactive oxygen species and vascular biology: implications in human hypertension

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