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

@article{Nishiyama2001SystemicAR,
  title={Systemic and Regional Hemodynamic Responses to Tempol in Angiotensin II–Infused Hypertensive Rats},
  author={Akira Nishiyama and Toshiki Fukui and Yoshihide Fujisawa and Matlubur Rahman and Run Tian and Shoji Kimura and Youichi Abe},
  journal={Hypertension: Journal of the American Heart Association},
  year={2001},
  volume={37},
  pages={77-83},
  url={https://api.semanticscholar.org/CorpusID:21542090}
}
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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NO-independent mechanism mediates tempol-induced renal vasodilation in SHR.

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...

34 References

Renoprotective effects of nitric oxide in angiotensin II-induced hypertension in the rat.

It is suggested that a compensatory increase in nitric oxide activity partially counteracts the vasoconstrictor influence of elevated ANG II levels to regulate renal hemodynamics and maintain cortical perfusion in the renal circulation.

Regional blood flow responses to acute ANG II infusion: effects of nitric oxide synthase inhibition.

The results indicate that the ability of NO to oppose ANG II-induced constriction is not homogeneous among regional circulations, and the constrictor effects of NOS inhibition and ANG II are additive in these circulations.

Interactive nitric oxide-angiotensin II influences on renal microcirculation in angiotensin II-induced hypertension.

It is suggested that in this model of hypertension, maintained nitric oxide production in afferent arterioles counteracts the enhanced afferentarteriolar reactivity that occurs in Ang II-induced hypertension.

Renal uptake of circulating angiotensin II in Val5-angiotensin II infused rats is mediated by AT1 receptor.

Role of renal nerves in afferent arteriolar reactivity in angiotensin-induced hypertension.

The results indicate that renal nerves contribute to the development of hypertension and to the enhanced afferent arteriolar responsiveness to Ang II elicited by chronic Ang II infusion.

Augmentation of intrarenal angiotensin II levels by chronic angiotensin II infusion.

The objective of this study was to investigate the singular role of elevated angiotensin II (ANG II) levels in the development of two-kidney, one-clip (2K1C) Goldblatt hypertension in the rat and…

Regulation of angiotensin II type 1 receptor mRNA and protein in angiotensin II-induced hypertension.

Results indicate that renal and liver AT1 receptor gene expression is maintained in Ang II-induced hypertension, and the failure to downregulate AT1 receptors mRNA and protein levels thus allows the sustained effects of chronic elevations inAng II to elicit progressive increases in arterial pressure.

Receptor-mediated intrarenal angiotensin II augmentation in angiotensin II-infused rats.

The results suggest that the tissue-specific elevations of intrarenal Ang II levels caused by chronic Ang II infusion are mediated by angiotensin type 1 receptor activation, which leads to either receptor-mediated internalization of Ang II, enhancement of intra RenalAng II formation, or both.

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.

Role of superoxide in angiotensin II-induced but not catecholamine-induced hypertension.

Hypertension caused by chronically elevated angiotensin II is mediated in part by .O2-, likely via degradation of endothelium-derived NO, and may contribute to vascular disease in high renin/angiotens in II states.

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