How Do Glucocorticoids Cause Hypertension: Role of Nitric Oxide Deficiency, Oxidative Stress, and Eicosanoids

Ong, Sharon L.H.; Whitworth, Judith A.

doi:10.1016/j.ecl.2011.01.010

Cited by 55 publications

(26 citation statements)

References 84 publications

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“…First, a growing body of evidence indicates that redox signaling plays a pivotal role in epigenetic regulation, including the methylation of CpG islands, and the modification of histone proteins and microRNAs [17]. A disturbed balance between NO and ROS is involved in the epigenetic regulation of genes implicated in control of BP in a variety of programmed hypertension models [18,19,20]; Second are studies of oxidative stress on glucocorticoid-induced hypertension [21]. The NO-ROS imbalance has been reported in several models of glucocorticoid-induced programmed hypertension [20,22,23,24,25,26,27]; Third are many reports that angiotensin II–induced oxidative stress plays an important role in the development of hypertension [6,28,29], whereas early blockade of the RAS has been shown to deprogram the inappropriately activated RAS and reduce oxidative stress to prevent the development of programmed hypertension [30,31]; Last, epidemiologic studies support that low birth weight and prematurity, both associated with reduced nephron endowment, are risk factors for hypertension in later life [32,33].…”

Section: Developmental Origins Of Hypertension: Focus On the Kidneymentioning

confidence: 99%

Targeting on Asymmetric Dimethylarginine-Related Nitric Oxide-Reactive Oxygen Species Imbalance to Reprogram the Development of Hypertension

Tain

Hsu

2016

IJMS

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Adult-onset diseases, including hypertension, can originate from early life, known as the developmental origins of health and disease (DOHaD). Because the developing kidney is vulnerable to early-life insults, renal programming is considered key in the developmental programming of hypertension. Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide (NO) synthase inhibitor, can regulate the NO–reactive oxygen species (ROS) balance, and is involved in the development of hypertension. Reprogramming interventions aimed at NO-ROS balance can be protective in both genetic and developmentally programmed hypertension. Here we review several emergent themes of the DOHaD approach regarding the impact of ADMA-related NO-ROS imbalance on programmed hypertension. We focus on the kidney in the following areas: mechanistic insights to interpret programmed hypertension; the impact of ADMA-related NO-ROS imbalance in both genetic and acquired animal models of hypertension; alterations of the renal transcriptome in response to ADMA in the developing kidney; and reprogramming strategies targeting ADMA-related NO-ROS balance to prevent programmed hypertension.

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Section: Developmental Origins Of Hypertension: Focus On the Kidneymentioning

confidence: 99%

Targeting on Asymmetric Dimethylarginine-Related Nitric Oxide-Reactive Oxygen Species Imbalance to Reprogram the Development of Hypertension

Tain

Hsu

2016

IJMS

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“…NO deficiency is strongly related to the redox imbalance [108]. Inducible nitric oxide synthase (iNOS), which is expressed exclusively under inflammatory condition to produce large amounts of prooxidative NO, is prominently expressed in gingival tissues with periodontitis [109].…”

Section: Possible Linking Pathways For the Association Between Hypmentioning

confidence: 99%

Association between Hypertension and Periodontitis: Possible Mechanisms

Leong

Baharin

et al. 2014

The Scientific World Journal

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This review is to examine the current literatures on the relationship between periodontitis and hypertension as well as to explore the possible biological pathways underlying the linkage between these health conditions. Hypertension is one of the major risk factors for cardiovascular diseases. Oxidative stress and endothelial dysfunction are among the critical components in the development of hypertension. Inflammation has received much attention recently and may contribute to a pivotal role in hypertension. Periodontitis, a chronic low-grade inflammation of gingival tissue, has been linked to endothelial dysfunction, with blood pressure elevation and increased mortality risk in hypertensive patients. Inflammatory biomarkers are increased in hypertensive patients with periodontitis. Over the years, various researches have been performed to evaluate the involvement of periodontitis in the initiation and progression of hypertension. Many cross-sectional studies documented an association between hypertension and periodontitis. However, more well-designed prospective population trials need to be carried out to ascertain the role of periodontitis in hypertension.

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“…Chronic administration of glucocorticoid, especially at supraphysiological doses, leads to elevated systolic blood pressure, in man and animals [1]. Increased vascular sensitivity to glucocorticoids has been also demonstrated in patients with essential hypertension [2].…”

Section: Introductionmentioning

confidence: 99%

Antioxidant Effects of Bovine Lactoferrin on Dexamethasone-Induced Hypertension in Rat

Safaeian

Zabolian

2014

ISRN Pharmacology

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Dexamethasone- (Dex-) induced hypertension is associated with enhanced oxidative stress. Lactoferrin (LF) is an iron-binding glycoprotein with antihypertensive properties. In this study, we investigated the effect of chronic administration of LF on oxidative stress and hypertension upon Dex administration. Male Wistar rats were treated by Dex (30 μg/kg/day subcutaneously) or saline for 14 days. Oral bovine LF (30, 100, 300 mg/kg) was given from day 8 to 14 in a reversal study. In a prevention study, rats received 4 days of LF treatment followed by Dex and continued during the test period. Systolic blood pressure (SBP) was measured using tail-cuff method. Thymus weight was used as a marker of glucocorticoid activity. Plasma hydrogen peroxide (H2O2) concentration and ferric reducing antioxidant power (FRAP) value were determined. Dexamethasone significantly increased SBP and plasma H2O2 level and decreased thymus and body weights. LF lowered (P < 0.01) and dose dependently prevented (P < 0.001) Dex-induced hypertension. LF prevented body weight loss and significantly reduced the elevated plasma H2O2 and increased FRAP values. Chronic administration of LF strongly reduced the blood pressure and production of ROS and improved antioxidant capacity in Dex-induced hypertension, suggesting the role of inhibition of oxidative stress as another mechanism of antihypertensive action of LF.

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How Do Glucocorticoids Cause Hypertension: Role of Nitric Oxide Deficiency, Oxidative Stress, and Eicosanoids

Cited by 55 publications

References 84 publications

Targeting on Asymmetric Dimethylarginine-Related Nitric Oxide-Reactive Oxygen Species Imbalance to Reprogram the Development of Hypertension

Targeting on Asymmetric Dimethylarginine-Related Nitric Oxide-Reactive Oxygen Species Imbalance to Reprogram the Development of Hypertension

Association between Hypertension and Periodontitis: Possible Mechanisms

Antioxidant Effects of Bovine Lactoferrin on Dexamethasone-Induced Hypertension in Rat

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