Arterial Pressure Response to the Antioxidant Tempol and ETB Receptor Blockade in Rats on a High-Salt Diet

@article{Williams2004ArterialPR,
  title={Arterial Pressure Response to the Antioxidant Tempol and ETB Receptor Blockade in Rats on a High-Salt Diet},
  author={Jan Michael Williams and Jennifer S Pollock and David M. Pollock},
  journal={Hypertension},
  year={2004},
  volume={44},
  pages={770-775},
  url={https://api.semanticscholar.org/CorpusID:6319537}
}
The data suggest that blood pressure lowering by tempol in rats on a high-salt diet may be unrelated to reductions in superoxide and that renal H2O2 may account for the limited ability of tempol to attenuate hypertension produced by ETB receptor blockade.
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Effects of tempol on altered metabolism and renal vascular responsiveness in fructose-fed rats.

Chronic but not acute tempol treatment enhances renal vascular responsiveness in fructose-fed rats and plays a crucial role in controlling renal vascular responses to adrenergic agonists in insulin-resistant rats.

NADPH Oxidase Inhibition Attenuates Oxidative Stress but Not Hypertension Produced by Chronic ET-1

Evidence is provided that chronic ET-1 infusion increases vascular NADPH oxidase-dependent superoxide production but does not account for chronic ET–1–induced hypertension.

Synergistic actions of enalapril and tempol during chronic angiotensin II-induced hypertension.

Superoxide-Dependent Hypertension in Male and Female Endothelin B Receptor–Deficient Rats

The results indicate that the early stages of salt-dependent hypertension produced by ETB receptor deficiency are dependent on superoxide and that the elevated pressure in the female rats may be due to elevated circulating levels of ET-1.

Endothelin ETB receptors contribute to sex differences in blood pressure elevation in angiotensin II hypertensive rats on a high‐salt diet

Female rats are more resistant to blood pressure increases induced by high salt (HS) intake or angiotensin (Ang) II infusion, and endothelin ETB receptors play a significantly greater beneficial role in protecting female compared with male rats against AngII‐induced hypertension.

Superoxide Contributes to Development of Salt Sensitivity and Hypertension Induced by Nitric Oxide Deficiency

It is suggested that enhancement of O2− activity during NO inhibition contributes to the development of salt sensitivity that is associated with NO-deficient hypertension.

Extrarenal ETB Plays a Significant Role in Controlling Cardiovascular Responses to High Dietary Sodium in Rats

It is found that ETB deficiency in the body is associated with renal injury and an impaired ability to excrete an Na load, and the effect of chronic ETA blockade affects blood pressure response to dietary Na.

Chronic High-Sodium Diet Increases Aortic Wall Endothelin-1 Expression in a Blood Pressure–Independent Fashion in Rats

The expression of ET-1 mRNA by the aortic wall is increased in response to chronic high dietary sodium in WKY rats in the absence of changes in arterial blood pressure.

Contrasting effects of intervention with ETA and ETB receptor antagonists in hypertension induced by angiotensin II and high-salt diet.

The results confirm the importance of ETA receptor signaling in maintaining AngII-HS hypertension and suggest that including ETB receptor blockade in therapeutic approaches to treating hypertension would be ineffective or even counterproductive.

Enhanced superoxide generation modulates renal function in ANG II-induced hypertensive rats.

It is demonstrated that enhanced generation of O2(-) modulates renal hemodynamic and tubular reabsorptive function, possibly leading to sodium retention and thus contributing to the pathogenesis of ANG II-induced hypertension.
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45 References

Evidence for endothelin involvement in the response to high salt.

The hypothesis that endothelin, through the ET(B) receptor, participates in blood pressure regulation in the response to salt loading is supported.

Tempol Lowers Blood Pressure and Sympathetic Nerve Activity But Not Vascular O2− in DOCA-Salt Rats

It is concluded that depressor responses and decreases in HR and RSNA caused by acute tempol treatment are caused by direct sympathetic nerve activity inhibition that is not accompanied by SOD-mimetic action in the aorta or vena cava.

ETA receptor blockade attenuates the hypertension but not renal dysfunction in DOCA-salt rats.

ETA receptors appear to play a role in the maintenance and development of DOCA-salt hypertension but not in the accompanying reduction of renal function.

Renal Sympathetic Nerve Responses to Tempol in Spontaneously Hypertensive Rats

It is suggested that augmented superoxide production contributes to the development of hypertension through activation of the sympathetic nervous system through the use of superoxide dismutase mimetic Tempol.

ETA Receptor Blockade Decreases Vascular Superoxide Generation in DOCA-Salt Hypertension

In vivo findings indicate that increased vascular superoxide production is associated with activation of the endothelin system through ETA receptors in DOCA-salt hypertension, in apparently blood pressure–independent fashion.

ETA receptor-mediated role of endothelin in the kidney of DOCA-salt hypertensive rats.

Antihypertensive effects of a novel endothelin-A receptor antagonist in rats.

BMS-182874 is a specific, orally active endothelin-A receptor antagonist that is efficacious in mineralocorticoid hypertension in rats but has less effect in sodium-replete and sodium-deplete SHR.

Roles of Oxidative Stress and AT1 Receptors in Renal Hemodynamics and Oxygenation in the Postclipped 2K,1C Kidney

The correction of oxidative stress in the 2K,1C model partially corrects renal cortical hypoxia and inefficient utilization of O2 for Na+ transport, independent of the fall in blood pressure.

Two-week administration of tempol attenuates both hypertension and renal excretion of 8-Iso prostaglandin f2alpha.

The SHR is a model of hypertension and renal vasoconstriction associated with oxidative stress and a role for oxygen radicals in the maintenance of hypertension inSHR is suggested.

Role of Reactive Oxygen Species in Endothelin-Induced Hypertension

The data indicate that formation of reactive oxygen species may play an important role in mediating hypertension induced by chronic elevations in endothelin.
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