NO dependency of RBF and autoregulation in the spontaneously hypertensive rat.

@article{Racasan2003NODO,
  title={NO dependency of RBF and autoregulation in the spontaneously hypertensive rat.},
  author={Simona Racasan and Jaap A. Joles and Peter Boer and Hein A. Koomans and Branko Braam},
  journal={American journal of physiology. Renal physiology},
  year={2003},
  volume={285 1},
  pages={
          F105-12
        }
}
In the spontaneously hypertensive rat (SHR), renal blood flow (RBF) has been reported to be very dependent on nitric oxide (NO); however, autoregulation is normal, albeit shifted to higher perfusion pressures. To test the hypothesis that in the SHR NO dependency of RBF autoregulation is diminished, we investigated RBF autoregulation in anesthetized young male SHR and normotensive Wistar-Kyoto (WKY) rats before and during acute intravenous NO synthase (NOS) inhibition with N(omega)-nitro-L… 
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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.
Nitric oxide, superoxide and renal blood flow autoregulation in SHR after perinatal L‐arginine and antioxidants
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It is hypothesized that perinatal supplementation by restoring dynamic NO release and/or decreasing superoxide dependency and would improve life‐long blood pressure regulation.
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In rats receiving angiotensin II, adding losartan to drinking water only induced transient increase in renal oxygenation, despite normalisation of arterial pressure, and in rats receivingAngiotensine II-induced hypertension, renal hypoxia is only a transient phenomenon during initiation of angiotENSin II- induced hypertension.
A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats.
TLDR
It is hypothesized that this approach to enhancing perinatal nitric oxide availability can be generalized to other models of genetic hypertension, for instance those associated with renal injury, and can ameliorate development of hypertension and renal injury in FHH rats.
Maintenance of Hypertensive Hemodynamics Does Not Depend on ROS in Established Experimental Chronic Kidney Disease
TLDR
Although oxidative stress markers were increased, MAP and RVR did not depend more on oxidative stress in CKD than in controls, and reactive oxygen species appear not to be important direct determinants of hypertensive renal hemodynamics in this model of established CKD.
Salt-resistant blood pressure and salt-sensitive renal autoregulation in chronic streptozotocin diabetes.
TLDR
Renal blood flow dynamics show strong contributions to autoregulation by both TGF and the myogenic mechanism and were not impaired by diabetes or by increased salt intake, confirming diabetic hyperfiltration and the salt paradox.
Sodium thiosulfate improves renal function and oxygenation in L-NNA-induced hypertension in rats.
RENAL FUNCTIONAL RESPONSES TO ISCHAEMIA–REPERFUSION INJURY IN NORMOTENSIVE AND HYPERTENSIVE RATS FOLLOWING NON‐SELECTIVE AND SELECTIVE CYCLO‐OXYGENASE INHIBITION WITH NITRIC OXIDE DONATION
  • S. Knight, E. Johns
  • Medicine, Biology
    Clinical and experimental pharmacology & physiology
  • 2008
TLDR
The results suggest that products of COX activity contribute to the renal responses to ischaemia–reperfusion injury, but in different ways, in SHRSP, which may reflect variations in renal prostaglandin and NO production in the hypertensive state.
Nitric Oxide Synthase Inhibition Induces Renal Medullary Hypoxia in Conscious Rats
TLDR
Chronic L‐NNA leads to decreased renal perfusion and sodium reabsorption efficiency, resulting in progressive medullary hypoxia, suggesting that juxtamedullary nephrons are potentially vulnerable to prolonged nitric oxide depletion.
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References

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