Renal Sympathetic Nerve Responses to Tempol in Spontaneously Hypertensive Rats

@article{Shokoji2003RenalSN,
  title={Renal Sympathetic Nerve Responses to Tempol in Spontaneously Hypertensive Rats},
  author={Takatomi Shokoji and Akira Nishiyama and Yoshihide Fujisawa and Hirofumi Hitomi and Hideyasu Kiyomoto and Norihiro Takahashi and Shoji Kimura and Masakazu Kohno and Youichi Abe},
  journal={Hypertension: Journal of The American Heart Association},
  year={2003},
  volume={41},
  pages={266-273},
  url={https://api.semanticscholar.org/CorpusID:14722089}
}
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.
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NO-independent mechanism mediates tempol-induced renal vasodilation in SHR.

In SHR, tempol has a significant renal vasodilator effect and that it normalizes the increased renovascular ANG II sensitivity and it is not likely that the elevated renal resistance and Ang II sensitivity in SHR are due to reactive oxygen species-induced quenching of nitric oxide.

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.

Acute antihypertensive action of Tempol in the spontaneously hypertensive rat.

The acute antihypertensive action of Tempol depends on the independent effects of potentiation of nitric oxide and inhibition of the peripheral SNS that involves the activation of K(ATP) channels.

Effects of tempol on baroreflex neural arc versus peripheral arc in normotensive and spontaneously hypertensive rats.

Although oxidative redox signaling affects arterial pressure (AP) regulation via modulation of vascular tone and sympathetic nerve activity (SNA), it remains unknown which effect plays a dominant…

Vascular Oxidative Stress Precedes High Blood Pressure in Spontaneously Hypertensive Rats

Data show that antioxidant treatment to reduce oxidative stress prevents the age-related development of high blood pressure in an animal model of genetic hypertension.

Systemic arterial pressure response to two weeks of Tempol therapy in SHR: involvement of NO, the RAS, and oxidative stress.

The data suggest that, in hypertensive individuals with endothelial damage and chronic NO deficiency, antioxidants may be able to reduce oxidative stress but not blood pressure, and that Tempol is unable to reduce MAP.

Activation of Vascular BK Channel by Tempol in DOCA-Salt Hypertensive Rats

It was found that tempol, but not tiron, dose-dependently relaxed mesenteric arteries (MA) in anesthetized sham and deoxycorticosterone acetate (DOCA)-salt hypertensive rats.

Superoxide Formation and Interaction with Nitric Oxide Modulate Systemic Arterial Pressure and Renal Function in Salt-Depleted Dogs

Analysis of responses to the intra-arterial infusion of an O2–-scavenging agent, tempol, in the denervated kidney of anesthetized salt-depleted dogs shows that low salt intake enhances O2- activity that influences renal and systemic hemodynamics and thus may contribute to the regulation of arterial pressure in the salt-restricted state.

Increased Reactive Oxygen Species in Rostral Ventrolateral Medulla Contribute to Neural Mechanisms of Hypertension in Stroke-Prone Spontaneously Hypertensive Rats

Results suggest that superoxide anions in the RVLM, which generate hydroxyl radicals, are increased inSHRSP and contribute to the neural mechanisms of hypertension in SHRSP.

Oxidative Stress Mediates the Stimulation of Sympathetic Nerve Activity in the Phenol Renal Injury Model of Hypertension

The studies suggest that central activation of the SNS in the phenol-renal injury model is mediated by increased reactive oxygen species in brain nuclei involved in the noradrenergic control of BP.
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32 References

Nitric oxide-independent effects of tempol on sympathetic nerve activity and blood pressure in DOCA-salt rats.

Tempol-induced depressor responses are mediated largely by NO-independent sympathoinhibition in sham and DOCA-salt rats, and there is an additional interaction between NO and tempol that contributes to depressorResponses inDOCA- salt rats.

Nitric oxide-independent effects of tempol on sympathetic nerve activity and blood pressure in normotensive rats.

In conclusion, depressor responses caused by tempol are mediated, partly, by sympathoinhibition in urethane-anesthetized, normotensive rats.

Role of nitric oxide in regulation of renal sympathetic nerve activity during hemorrhage in conscious rats.

The results indicate that NO modulated HR and RSNA responses to hemorrhage but did not directly affect the baroreceptor reflex arch, suggesting it can be assumed that No modulated thebaroreflex function by altering the secretion of vasopressin induced by hemorrhage.

Systemic and Regional Hemodynamic Responses to Tempol in Angiotensin II–Infused Hypertensive Rats

The results suggest that in this model of hypertension, oxidative stress may have contributed to the alterations in systemic blood pressure and regional vascular resistance through inactivation of NO.

Normalization of blood pressure and renal vascular resistance in SHR with a membrane-permeable superoxide dismutase mimetic: role of nitric oxide.

The data implicate O2- in the hypertension of SHR in vivo and suggest that the antihypertensive action of tempol depends on NO synthesis presumably because O 2- inactivates NO and thus diminishes its vasodilatory actions.

Central infusion of L-arginine or superoxide dismutase does not alter arterial pressure in SHR.

The hypothesis that chronic L-arginine deficiency or the enhanced degeneration of NO by superoxide radicals in the central nervous system contributes to the maintenance of arterial pressure in SHR is not supported.

Enhanced superoxide anion formation in vascular tissues from spontaneously hypertensive and desoxycorticosterone acetate-salt hypertensive rats

An enhanced ⋅ O2− formation resulting from an increased NADH oxidase activity was found in aorta from SHR and DOCA-HT rats, suggesting that the oxidative stress might contribute to the development of hypertension.

Chronic treatment with a superoxide dismutase mimetic prevents vascular remodeling and progression of hypertension in salt-loaded stroke-prone spontaneously hypertensive rats.

Superoxide anion production is increased in a model of genetic hypertension: role of the endothelium.

O2- generation is increased in SHRSP and that the tissue and enzymatic sources of this excess O2- appear to be the endothelium and eNOS, respectively.

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.

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