The anti-oxidant Tempol reverses and partially prevents adrenocorticotrophic hormone-induced hypertension in the rat

Zhang, Yi; Jang, R.; Mori, Trevor A.; Croft, Kevin D.; Schyvens, Christopher G.; McKenzie, Katja U.S.; Whitworth, Judith A.

doi:10.1097/00004872-200308000-00015

Cited by 44 publications

(35 citation statements)

References 38 publications

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“…In dexamethasone-induced hypertension among rats, this agent was shown to lower systolic blood pressure as well as restore plasma NO levels, without any effect on oxidative markers in the plasma. Similar experimental settings revealed N-acetylcysteine treatment having partially preventing but not reversing properties on GC-induced hypertension in comparison to what has been shown for tempol [91].…”

Section: Response To Antioxidants and Anti-inflammatory Agentssupporting

confidence: 64%

“…Antioxidants and anti-inflammatory agents such as tempol, apocynin, N-acetylcysteine, folic acid and atorvastatin can prevent and partially reverse GCs-induced hypertension in vivo [87][88][89][90][91][92]. Therefore, these substances represent promising candidates for prevention and treatment of increased systolic blood pressure induced by long-term and high-dosage GC treatment.…”

Section: Response To Antioxidants and Anti-inflammatory Agentsmentioning

confidence: 99%

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Role of Endothelial Nitric Oxide Synthase in Glucocorticoid- Induced Hypertension: An Overview of Experimental Data

Blecharz-Lang¹,

Burek²

2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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Imbalances in the synthesis or in the bioavailability of nitric oxide (NO), the freely diffusible vasodilator, in myocardial endothelial cells were demonstrated to be crucial in the development of hypertension. Glucocorticoids (GCs) are widely used as immunomodulators. One of the numerous side effects of GC therapy is hypertension arising from reduced release of the endothelium-derived NO. GCs can modulate NO synthesis by targeting the genes involved in it, like nitric oxide synthase (NOS) and guanosine triphosphate (GTP) cyclohydrolase-1 (GTPCH-1). This chapter will give an overview on the impact of GCs on NO synthesis and signalling in animal models as well as in in vitro cell culture models. Moreover, strategies for preventing or neutralizing side effects of long-term GC therapy will be discussed.

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Section: Response To Antioxidants and Anti-inflammatory Agentssupporting

confidence: 64%

Section: Response To Antioxidants and Anti-inflammatory Agentsmentioning

confidence: 99%

Role of Endothelial Nitric Oxide Synthase in Glucocorticoid- Induced Hypertension: An Overview of Experimental Data

Blecharz-Lang¹,

Burek²

2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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“…NO and ROS interact at rates greater than that of superoxide removal by superoxide dismutase (18) and thus ROS effectively reduces NO bioavailability. Our group has previously shown that tempol, a superoxide scavenger (19) and ramipril (20) (an inhibitor of angiotensin II stimulated NADPH oxidase production of ROS) can reduce elevated BP in ACTH-treated rats. Furthermore, in a model of angiotensin II slow pressor response in mice, angiotensin II elevated BP and increased urinary 8-isoprostane prostaglandin levels (a marker of whole animal oxidative stress and lipid peroxidation) (21).…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic Effects of the Nitric Oxide Donor DETA/NO in Mice

Schyvens

Cowden

Zhang

et al. 2004

Clinical and Experimental Hypertension

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(Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA/NO) is a recently synthesized member of NO-releasing, polyamine zwitterions, the so-called NONOates, that spontaneously liberate NO in aqueous solutions. The aim of this study was to determine the hemodynamic effects of DETA/ NO in normotensive and hypertensive mice. Male Swiss Outbred mice were implanted with TA11PA-C20 blood pressure devices (Data Sciences International, USA). After recovery (7-10 days), blood pressure was monitored for 10 days while mice were receiving saline (0.1 ml/20 g/day, s.c.). Mice were then treated every four hours for 1 day with either DETA/NO 60 mg/kg i.p. or the inactive metabolite, diethylenetriamine 38 mg/kg (molar equivalent) i.p. After a 2 week wash-out period, mice were treated with adrenocorticotrophic hormone (ACTH: 500 microg/kg/day, s.c.) for 10 days and re-challenged with DETA/NO or diethylenetriamine. Results were expressed as mean +/- SEM. After 10 days of saline treatment, baseline systolic and diastolic blood pressure (BP) were similar for animals subsequently receiving DETA/NO or the amine (123 +/- 1/95 +/- 3 and 124 +/- 1/92 +/- 0.2 mmHg) respectively. DETA/NO induced a profound fall in BP [Systolic: 74 +/- 4 mmHg (-40 +/- 3%); Diastolic: 46 +/- 4 mmHg (-52 +/- 4%)] and an increase in heart rate [729 +/- 33 bpm (32 +/- 2%)] within the first 80 minutes. Diethylenetriamine had no effect. ACTH treatment increased BP in both groups (137 +/- 16/108 +/- 12 and 161 +/- 1/142 +/- 1 mmHg) respectively. DETA/ NO induced a profound fall in blood pressure [Systolic: 92 +/- 11 mmHg (-32 +/- 7%); Diastolic: 68 +/- 10 mmHg (-35 +/- 10%)] and an increase in heart rate [613 +/- 36 bpm (18 +/- 6%)] within the first 80 minutes. Again diethylenetriamine had no significant effect. There was no significant effect on body weight with any treatment. Thus DETA/NO has potent blood pressure lowering effects in both normotensive and hypertensive mice.

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“…Plasma nitrate/ nitrite (NOx) levels are low in GC-induced hypertension, and supplementation with L-arginine restored plasma NOx concentrations in ACTH treated rats to control levels (7). 74 C. K. Mondo et al GC also enhance generation of free radicals, in particular reactive oxygen species (ROS) (8)(9)(10). ROS are produced by several enzymes that may contribute to the oxidative load during hypertension.…”

Section: Introductionmentioning

confidence: 99%

N-Acetylcysteine Antagonizes the Development But Does Not Reverse ACTH-Induced Hypertension in the Rat

Mondo

Zhang

Possamai

et al. 2006

Clinical and Experimental Hypertension

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We investigated the effect of antioxidant N-acetylcysteine (NAC) on adrenocorticotropic hormone (ACTH)-hypertension. Male Sprague-Dawley rats received NAC (10 mg/L) or water 4 days before ACTH/saline treatment for 13 days (prevention study). In a reversal study, NAC commenced on day 8 of ACTH/saline treatment and continued for 5 days. ACTH increased systolic blood pressure (SBP) in water drinking rats (111 +/- 1 to 131 +/- 3 mmHg, p < 0.001). In the prevention study, NAC + ACTH increased SBP (108 +/- 2 to 120 +/- 2 mmHg, p < 0.001) but less than ACTH alone (p' < 0.05). In the reversal study, NAC had no significant effect (132 +/- 4 to 124 +/- 3 mmHg, ns). Thus, NAC partially prevented but did not reverse ACTH-induced hypertension.

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The anti-oxidant Tempol reverses and partially prevents adrenocorticotrophic hormone-induced hypertension in the rat

Abstract: ACTH-induced hypertension in the rat is associated with increased oxidative stress. Tempol treatment reversed, and pretreatment partially prevented ACTH-induced hypertension, independent of improvement in systemic oxidative stress.

Cited by 44 publications

References 38 publications

Role of Endothelial Nitric Oxide Synthase in Glucocorticoid- Induced Hypertension: An Overview of Experimental Data

Role of Endothelial Nitric Oxide Synthase in Glucocorticoid- Induced Hypertension: An Overview of Experimental Data

Hemodynamic Effects of the Nitric Oxide Donor DETA/NO in Mice

N-Acetylcysteine Antagonizes the Development But Does Not Reverse ACTH-Induced Hypertension in the Rat

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