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

@article{Kagiyama2000CentralIO,
  title={Central infusion of L-arginine or superoxide dismutase does not alter arterial pressure in SHR.},
  author={Shuntaro Kagiyama and Takuya Tsuchihashi and Isao Abe and Kiyoshi Matsumura and Masatoshi Fujishima},
  journal={Hypertension research : official journal of the Japanese Society of Hypertension},
  year={2000},
  volume={23 4},
  pages={
          339-43
        },
  url={https://api.semanticscholar.org/CorpusID:29810353}
}
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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12 Citations

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.

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.

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.

Does central nitric oxide elicit pulmonary hypertension in conscious rats?

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.

Overexpression of Inducible Nitric Oxide Synthase in Rostral Ventrolateral Medulla Causes Hypertension and Sympathoexcitation via an Increase in Oxidative Stress

It is suggested that overexpression of iNOS in the RVLM increases blood pressure via activation of the sympathetic nervous system, which is mediated by an increase in oxidative stress.

Effects of Local Administrations of Tempol and Diethyldithio-Carbamic on Peripheral Nerve Activity

The results suggest that reactive oxygen species play a role in the regulation of peripheral sympathetic nerve activity, and that at least part of this mechanism is mediated through voltage-gated potassium channels.

The effect of tempol on endothelium-dependent vasodilatation and blood pressure.

Central interactions of aldosterone and angiotensin II in aldosterone- and angiotensin II-induced hypertension.

The results suggest that ANG II and Aldo interact in the brain in a mutually cooperative manner such that the functional integrity of both brain AT1R and MR are necessary for hypertension to be induced by either systemic ANG II or Aldo.

26 References

Enhanced depressor response to nitric oxide in the rostral ventrolateral medulla of spontaneously hypertensive rats.

The results suggest that the L-arginine-NO pathway in the rostral ventrolateral medulla of adult spontaneously hypertensive rats (SHR) is impaired and that this impairment may contribute to the increase in arterial pressure in this animal model of genetic hypertension.

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.

Chronic L-arginine administration attenuates cardiac hypertrophy in spontaneously hypertensive rats.

Nitric oxide inhibits proliferation and migration of vascular smooth muscle cells and contractility of cardiomyocytes in vitro. In spontaneously hypertensive rats (SHR), evidence suggests intrinsic…

Chronic inhibition of nitric oxide in central nervous system does not cause hypertension.

It is suggested that endogenous NO in the central nervous system, at least as a whole, may not affect the systemic hemodynamics of chronic unanesthetized rats and plasma norepinephrine levels did not differ between the two groups of rats at either low- or high-dose treatment.

L-arginine abrogates salt-sensitive hypertension in Dahl/Rapp rats.

L-arginine and L-citrulline increased production of NO and prevented salt-sensitive hypertension in Dahl/Rapp rats and did not alter the development of hypertension in spontaneously hypertensive rats.

Role of nitric oxide in the nucleus of the solitary tract of rats

Central and peripheral mechanisms involved in hypertension induced by chronic inhibition of nitric oxide synthase in rats.

Results indicate that L-NAME-induced hypertension is associated with a deficiency of nitric oxide, both peripherally and centrally.

A central nervous system action of nitric oxide in blood pressure regulation.

The findings indicate that L-NMA acts centrally by an ARG-reversible mechanism in the anesthetized rat to stimulate sympathetic nerve activity and suggest that one such function would be the central regulation of sympathetic outflow and hence, BP.

NG-methyl-L-arginine, an inhibitor of L-arginine-derived nitric oxide synthesis, stimulates renal sympathetic nerve activity in vivo. A role for nitric oxide in the central regulation of sympathetic tone?

NMA, a selective inhibitor of NO synthesis from L-arginine, was investigated on sympathetic renal nerve activity, blood pressure, and heart rate in the anesthetized rat and baroreceptor deafferentation markedly altered these responses to NMA.

Nitric oxide influences ventrolateral medullary mechanisms of vasomotor control in the cat

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