N-acetylcysteine improves nitric oxide and α-adrenergic pathways in mesenteric beds of spontaneously hypertensive rats

Girouard, Hélène; Chulak, Chantal; Wu, Lin‐Sheng; LeJossec, Mireille; Champlain, Jacques de

doi:10.1016/s0895-7061(03)00863-x

Cited by 54 publications

(29 citation statements)

References 22 publications

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“…The renal vascular resistance was calculated and no difference was found between the animals pretreated with NAC compared to those receiving no pretreatment. This observation is in opposition to previous reports, where interactions with the renin-angiotensin system [40] and the formation of nitric oxide [20,34,41] were believed to be responsible for the hemodynamic effects of NAC. Heyman et al [24] could show that the strongest vasodilatory effect of NAC was noted in animals with the most intense renal vasoconstriction; no effects were found in intact animals.…”

Section: Discussioncontrasting

confidence: 99%

Effects of N-Acetylcysteine on Renal Hemodynamics in Contrast Media-Induced Nephropathy

Krzossok¹,

Braun²,

Weiss³

et al. 2011

Kidney Blood Press Res

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Background: N-acetylcysteine (NAC) has been proposed to prevent radiocontrast nephropathy in high-risk patients. Methods: The effect of single-dose and prolonged administration of NAC before application of either the ionic, high-osmolar radiocontrast agent diatrizoate sodium (DTZ) or the nonionic, low-osmolar radiocontrast agent iohexol (IOH) in a rat model combining uninephrectomy, salt depletion, and administration of indomethacin was explored. Arterial blood pressure and total, cortical, and medullary blood flow were continuously recorded in anesthetized Sprague-Dawley rats. Results: NAC had no effect on renal hemodynamics in control rats. Both DTZ and IOH induced biphasic changes in renal blood flow and cortical renal blood flux and persistently reduced medullary blood flux. Neither single-dose nor prolonged administration of NAC prevented the hemodynamic changes following administration of DTZ or IOH, respectively. Acute prophylactic administration of NAC prevented increased urinary ET excretion after injection of IOH and, to a smaller degree, of DTZ. Both an ionic, high-osmolar (DTZ) and a nonionic, low-osmolar (IOH) radiocontrast agent induce marked changes in renal hemodynamics in salt-depleted rats treated with indomethacin. Conclusions: Renal perfusion is not affected by NAC application in a model of experimental contrast nephropathy in rats. Other effects of NAC might thus account for the presumed renoprotective properties.

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Section: Discussioncontrasting

confidence: 99%

Effects of N-Acetylcysteine on Renal Hemodynamics in Contrast Media-Induced Nephropathy

Krzossok¹,

Braun²,

Weiss³

et al. 2011

Kidney Blood Press Res

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“…[46][47][48] The antihypertensive effect of NAC was quite likely mediated by increased NOdependent vasodilation. 49 In this study, an infusion of NAC, an antioxidant and glutathione precursor, prevented the increase in oxidative stress, restored NO availability and prevented the elevation of arterial BP and heart rate through mechanism(s) that may involve the restoration of NO bioavailability and antioxidant capacity.…”

Section: Discussionmentioning

confidence: 69%

Role of oxidative stress in elevated blood pressure induced by high free fatty acids

Wang

Hou

et al. 2009

Hypertens Res

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The aim of the study is to investigate the possible mechanism of oxidative stress in the high free fatty acids (FFAs)-induced hypertension. Male Sprague-Dawley rat models were established and classified into three groups, namely the control group (NC group), the FFA group, and the N-acetylcysteine (NAC) group. Blood pressure (BP) was recorded. An organ chamber experiment was performed to determine endothelium-dependent/-independent vasodilation (EDV/EIV). Reactive oxygen species (ROS), nitrotyrosine, reduced glutathione hormone (GSH) and NO 2 À /NO 3 À levels were measured in plasma. Endothelial nitric oxide synthase (eNOS) mRNA expression in endothelial cells was evaluated by real-time PCR. The following results were observed: (1) In the FFA group, BP increased after 4 h infusion of Intralipid+heparin. In the NAC group, systolic and diastolic BP remained the same. (2) In the FFA group, the aortic rings tended to show impaired EDV in response to acetylcholine (ACh). There was no difference of EDV response in the NAC and NC groups. (3) In the FFA group, NO 2 À /NO 3 À levels were significantly reduced, and eNOS mRNA expression and activity were significantly decreased compared with the NC group. NAC administration increased eNOS mRNA expression and activity. (4) ROS and nitrotyrosine concentrations in the FFA group were higher than in the NC group, and GSH concentrations in the FFA group were lower than in the NC group. Elevated FFAs can induce elevated BP, potentially through FFA-induced impairment of EDV resulting from decreased eNOS mRNA expression and activity. Oxidative stress may also play an important role in potential mechanisms of this high FFA-induced elevated BP.

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“…NAC has been shown to have vasodilatory actions in a number of vascular beds. For example, NAC treatment improved blood flow in ex vivo placentas from preeclamptic women [29] and decreased MAP in spontaneously hypertensive rats [30] . In addition, NAC has been shown to potentiate vasodilation in coronary arteries and the peripheral circulation of adult humans [31] .…”

Section: Discussionmentioning

confidence: 99%

The Anti-Inflammatory Agent N-Acetyl Cysteine Exacerbates Endotoxin-Induced Hypoxemia and Hypotension and Induces Polycythemia in the Ovine Fetus

et al. 2010

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Background: Lipopolysaccharide (LPS) delivered acutely to the ovine fetus induces cerebral white matter injury and brain inflammation. N-acetyl cysteine (NAC) is potentially neuroprotective as it blocks the production of inflammatory cytokines and increases glutathione levels; however, it is unknown whether NAC affects the physiological status of the fetus already exposed to an inflammatory environment. Objectives: Our objective was to determine whether NAC influences the physiological effects of LPS exposure in the ovine fetus. Methods: Catheterized fetal sheep underwent one of four treatments (saline, n = 6; LPS, n = 6; LPS + NAC, n = 6; NAC, n = 3) on 5 consecutive days from 95 days of gestation (term ∼147 days). Fetal arterial pressure and heart rate were recorded and blood samples collected. Results: LPS administration resulted in fetal hypoxemia and hypotension; simultaneous treatment with NAC exacerbated these effects and induced polycythemia. NAC treatment alone had no effect on the fetus. Conclusion: In the presence of LPS, NAC compromises fetal physiological status, suggesting that it may not be a suitable antenatal treatment for a fetus with evidence of inflammation.

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N-acetylcysteine improves nitric oxide and α-adrenergic pathways in mesenteric beds of spontaneously hypertensive rats

Abstract: The increase in NO-mediated vasodilator tone and the possible decrease in adrenergic vasoconstriction induced by NAC treatment in SHR could explain the hypotensive effect of NAC in this model of hypertension.

Cited by 54 publications

References 22 publications

Effects of N-Acetylcysteine on Renal Hemodynamics in Contrast Media-Induced Nephropathy

Effects of N-Acetylcysteine on Renal Hemodynamics in Contrast Media-Induced Nephropathy

Role of oxidative stress in elevated blood pressure induced by high free fatty acids

The Anti-Inflammatory Agent N-Acetyl Cysteine Exacerbates Endotoxin-Induced Hypoxemia and Hypotension and Induces Polycythemia in the Ovine Fetus

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