Effect of a high-salt diet on oxidant enzyme activity in skeletal muscle microcirculation.

@article{Lenda2002EffectOA,
  title={Effect of a high-salt diet on oxidant enzyme activity in skeletal muscle microcirculation.},
  author={Deborah M. Lenda and Matthew A. Boegehold},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2002},
  volume={282 2},
  pages={
          H395-402
        }
}
  • D. M. Lenda, M. Boegehold
  • Published 1 February 2002
  • Biology
  • American journal of physiology. Heart and circulatory physiology
Increased salt intake attenuates the endothelium-dependent dilation of skeletal muscle arterioles by abolishing local nitric oxide (NO) activity. There is evidence of oxidative stress in arteriolar and venular walls of rats fed a high-salt diet, and depressed arteriolar responses to acetylcholine (ACh) in these rats are reversed by scavengers of reactive oxygen species (ROS). In this study, we tested the hypothesis that this salt-dependent increase in microvascular ROS and the resulting… 
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High salt intake reduces endothelium-dependent dilation of mouse arterioles via superoxide anion generated from nitric oxide synthase.
  • T. Nurkiewicz, M. Boegehold
  • Biology, Chemistry
    American journal of physiology. Regulatory, integrative and comparative physiology
  • 2007
TLDR
It is suggested that a high salt diet promotes increased generation of superoxide anion from NOS in the murine skeletal muscle microcirculation, thus impairing endothelium-dependent dilation through reduced NO bioavailability.
Reduced Arteriolar Responses to Skeletal Muscle Contraction after Ingestion of a High Salt Diet
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The findings suggest that increased oxidant activity in the arteriolar network of salt-fed rats is not due to accumulation of superoxide anion and that neither this oxidantactivity nor reduced NO availability can account for the blunted active arteriolaar dilation in rats fed a 4% salt diet.
Effect of High-Salt Diet on Vascular Relaxation and Oxidative Stress in Mesenteric Resistance Arteries
TLDR
The data suggest that the elevated production of superoxide by NADPH oxidase and xanthine/xanthine oxidase contribute to elevated basal superoxide levels, reduced NO release and impaired vascular relaxation in mesenteric resistance arteries of rats fed HS diet.
High salt intake shifts the mechanisms of flow-induced dilation in the middle cerebral arteries of Sprague-Dawley rats.
TLDR
In vivo reactive oxygen species scavenging restores flow-induced dilation in HS diet-fed rats and ameliorates HS-induced increases in the transcription factor hypoxia-inducible factor-1α and expression of its downstream target genes.
The Effect of High Salt Intake on Endothelial Function: Reduced Vascular Nitric Oxide in the Absence of Hypertension
TLDR
Additional studies are needed to further elucidate the mechanisms, both at the systemic level and within the vascular wall, that trigger these salt-induced deficits in endothelial function, and to further clarify how the attendant loss of NO may disrupt tissue blood flow regulation and ultimately lead to adverse cardiovascular events.
Reduced Angiotensin II and Oxidative Stress Contribute to Impaired Vasodilation in Dahl Salt-Sensitive Rats on Low-Salt Diet
TLDR
Data indicate that exposure to chronically low Ang II levels leads to impaired vascular relaxation in SS rats, even when the animals are on LS diet and normotensive.
Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension.
TLDR
The beneficial influence of dietary sodium restriction on target organ damage induced by angiotensin II is independent of arterial pressure reduction and possibly related to attenuation of the prooxidant effect of the peptide.
Microvascular Structure and Function in Salt‐Sensitive Hypertension
TLDR
The salt‐induced exacerbation of hypertension in Dahl rats is due to a uniform increase in hemodynamic resistance throughout most of the peripheral vasculature, and this effect must also be considered when evaluating microvascular changes and their functional consequences in salt‐sensitive hypertension.
Low-dose angiotensin II infusion restores vascular function in cerebral arteries of high salt-fed rats by increasing copper/zinc superoxide dimutase expression.
TLDR
Prevention of salt-induced ANG II suppression prevents vascular dysfunction in the cerebral circulation by preventing the downregulation of Cu/Zn SOD and vascular oxidant stress that normally occurs with HS diet.
Apocynin and Tempol ameliorate dietary sodium-induced declines in cutaneous microvascular function in salt-resistant humans.
TLDR
Local infusion of apocynin and Tempol improved microv vascular function in salt-resistant adults on a high-salt diet, providing evidence that reactive oxygen species contribute to impairments in microvascular function from high salt.
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