DOI:10.1152/ajpheart.2001.281.2.h975 - Corpus ID: 12881433
Nitric oxide-independent effects of tempol on sympathetic nerve activity and blood pressure in normotensive rats.
@article{Xu2001NitricOE, title={Nitric oxide-independent effects of tempol on sympathetic nerve activity and blood pressure in normotensive rats.}, author={H Xu and Gregory D. Fink and A. Chen and Stephanie W. Watts and James J. Galligan}, journal={American journal of physiology. Heart and circulatory physiology}, year={2001}, volume={281 2}, pages={ H975-80 }, url={https://api.semanticscholar.org/CorpusID:12881433} }
- H. Xu, G. Fink, J. Galligan
- Published in American Journal of… 2001
- Medicine
In conclusion, depressor responses caused by tempol are mediated, partly, by sympathoinhibition in urethane-anesthetized, normotensive rats.
45 Citations
45 Citations
Renal Sympathetic Nerve Responses to Tempol in Spontaneously Hypertensive Rats
- T. ShokojiA. Nishiyama Y. Abe
- Medicine
- 2003
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.
Tempol Lowers Blood Pressure and Sympathetic Nerve Activity But Not Vascular O2− in DOCA-Salt Rats
- Hui XuG. FinkJ. Galligan
- Medicine
- 2004
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.
Central Tempol alters basal sympathetic nerve discharge and attenuates sympathetic excitation to central ANG II.
It is demonstrated that icv Tempol administration influences central sympathetic neural circuits in a dose-dependent manner and attenuates SND responses to central ANG II infusion.
Enhanced angiotensin II-mediated central sympathoexcitation in streptozotocin-induced diabetes: role of superoxide anion.
- K. PatelW. MayhanK. BidaseeHong Zheng
- Medicine, Biology
- 2011
The concept that superoxide anion contributes to an enhanced ANG II-mediated signaling in the paraventricular nucleus (PVN) involved with the exaggerated sympathoexcitation in diabetes is supported.
Systemically administered tempol reduces neuronal activity in paraventricular nucleus of hypothalamus and rostral ventrolateral medulla in rats
- Shun-Guang WeiZhi-hua ZhangYang YuR. Felder
- Biology, Medicine
- 2009
It is suggested that systemically administered tempol acts upon neurons in paraventricular nucleus and RVLM to reduce BP, HR and RSNA, perhaps by reducing the influence of reactive oxygen species in those regions.
Oxidative stress and neuronal NOS activity: putative determinants of rapid blood pressure increase after renal denervation in anesthetized rats.
- A. WalkowskaJ. SadowskiE. Kompanowska-Jezierska
- Biology, Environmental Science
- 2013
It is proposed that enhanced afferent impulsation from intrarenal chemoreceptors related to oxidative stress in the kidney was the background for acute BP increase after DNX, triggered by a release of brain sympatho-excitatory centers from inhibition by renal afferents, and followed by widespread sympathetic cardiovascular stimulation.
Oxidative Stress and Neuronal Nos Activity: Putative Determinants of Rapid Blood Pressure Increase after Renal Denervation in Anaesthetised Rats Running Title: Reflex Blood Pressure Rise after Renal Denervation in the Rat
- A. WalkowskaJ. SadowskiElśbieta Kompanowska-JezierskaA. Walkowska
- Biology, Environmental Science
It is proposed that enhanced afferent impulsation from intrarenal chemoreceptors related to oxidative stress in the kidney was the background for acute BP increase after DNX, triggered by a release of brain sympatho-excitatory centres from inhibition by renal afferents.
Mechanisms of Hypertension Induced by Nitric Oxide (NO) Deficiency: Focus on Venous Function
- Keshari M. ThakaliYanny E LauG. FinkJ. GalliganAlex F. ChenS. Watts
- Environmental Science, Medicine
- 2006
The data suggest that while NO deficiency increases oxidative stress and sympathetic activity in both arterial and venous vessels, the impact on veins does not make a major contribution to this form of hypertension.
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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.
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Systemic and Regional Hemodynamic Responses to Tempol in Angiotensin II–Infused Hypertensive Rats
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- Medicine
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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.
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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.
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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.
Effects of induced hypothermia on renal sympathetic nerve activity and baroreceptor reflex in urethane-anesthetized rabbits
Hemodynamics and RSNA during induced hypothermia are regulated by mechanisms other than the baroreceptor reflex system, possibly the dermal cold receptors.
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