Sympathetic activity in early renal posttransplantation hypertension in rats.

@article{Grisk2000SympatheticAI,
  title={Sympathetic activity in early renal posttransplantation hypertension in rats.},
  author={Olaf Grisk and B A Frey and Amanda M. Uber and Richard A. Rettig},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2000},
  volume={279 5},
  pages={
          R1737-44
        }
}
  • O. Grisk, B. Frey, +1 author R. Rettig
  • Published 1 November 2000
  • Biology, Medicine
  • American journal of physiology. Regulatory, integrative and comparative physiology
The contribution of elevated sympathetic activity to the development of renal posttransplantation hypertension was investigated. F1 hybrids (F1H) from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were transplanted with either an SHR or an F1H kidney and bilaterally nephrectomized. Three weeks after transplantation, sympathetic activity was assessed by measuring adrenal tyrosine hydroxylase (TH) mRNA content and recording splanchnic nerve activity (SNA) in conscious animals… 
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16 Citations
Background Citations
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Methods Citations
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Results Citations
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16 Citations

Citation Type

Citation Type

Long-term arterial pressure in spontaneously hypertensive rats is set by the kidney
TLDR
In SHR, arterial Pressure can be normalized by a kidney graft from normotensive histocompatible donors and the genetic predisposition of the recipients to hypertension does not modify the rate and the extent of the arterial pressure rise induced by an SHR kidney graft.
Sympathetic-renal interaction in chronic arterial pressure control.
TLDR
Generalized reduction in sympathetic tone resets the kidney-fluid system to reduced MAP and blunts the extent of arterial pressure rise induced by an SHR kidney graft.
Analysis of arterial pressure regulating systems in renal post-transplantation hypertension
TLDR
It is concluded that post-transplantation hypertension in recipients of an SHR kidney is due to mechanisms other than those investigated in the present study, which could be involved in the genesis of this form of hypertension.
Sympatho‐renal interactions in the determination of arterial pressure: role in hypertension
  • O. Grisk
  • Medicine, Biology
    Experimental physiology
  • 2005
TLDR
It is concluded that chronic non‐adapting changes in sympathetic activity modulate the degree to which renal mechanisms can cause hypertension in SHRs.
Interactions between the sympathetic nervous system and the kidneys in arterial hypertension.
Renal Transplantation Studies in Genetic
TLDR
These findings, which were the results of animal experiments and mathematical modeling, contributed to direct attention to renal physiology and pathophysiology in the field of hypertension research.
Elevated renal norepinephrine in proANP gene-disrupted mice is associated with increased tyrosine hydroxylase expression in sympathetic ganglia
The kidney as a determinant of genetic hypertension: evidence from renal transplantation studies.
TLDR
The results and implications of clinical and experimental renal transplantation studies in primary hypertension in humans and genetic hypertension in animals that have been published to date are discussed.
Mechanisms of blood pressure variability-induced cardiac hypertrophy and dysfunction in mice with impaired baroreflex.
TLDR
More frequent blood pressure rises in subjects with high blood pressure variability activate mechanosensitive and autocrine pathways leading to cardiac hypertrophy and dysfunction even in the absence of hypertension.
Frequency modulation of mesenteric and renal vascular resistance.
  • O. Grisk, H. Stauss
  • Biology, Medicine
    American journal of physiology. Regulatory, integrative and comparative physiology
  • 2002
TLDR
Frequency modulation of low-frequency vasomotions in individual vascular beds does not cause significant blood pressure oscillations at additional frequencies, and the data suggest that sympathetic modulation of mesenteric vascular resistance can initiate blood pressurescillations at slightly higher frequencies than sympathetic stimulation of renal vascular resistance.
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References

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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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