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Decrease of endothelial nitric oxide synthase in stroke-prone spontaneously hypertensive rat cerebral cortex.

S Kimoto-Kinoshita1, S Nishida, T T Tomura

  • 1Department of Biochemistry & Oncology, Kinki University School of Medicine, Osaka-sayama, 589-8511, Osaka, Japan. saori@med.kindai.ac.jp

Neuroscience Letters
|July 6, 2000
PubMed
Summary
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Endothelial nitric oxide synthase (eNOS) protein decreased in stroke-prone spontaneously hypertensive rat cerebral cortex, suggesting its alteration is linked to stroke development. Neuronal NOS (nNOS) protein levels remained unchanged.

Area of Science:

  • Neuroscience
  • Cardiovascular Research
  • Biochemistry

Background:

  • Previous studies indicated decreased constitutive nitric oxide synthase (cNOS) activity and increased oxidative stress in the cerebral cortex (CC) of 31-week-old stroke-prone spontaneously hypertensive rats (SHRSP).
  • Nitric oxide synthase (NOS) exists in multiple isoforms, including neuronal NOS (nNOS) and endothelial NOS (eNOS), which play critical roles in regulating vascular function and neuronal activity.

Purpose of the Study:

  • To investigate the protein expression levels of nNOS and eNOS in the cerebral cortex of SHRSP.
  • To determine the association between specific cNOS isoform alterations and stroke development in SHRSP.

Main Methods:

  • Western blot analysis was employed to quantify the protein amounts of nNOS and eNOS in the cerebral cortex of 31-week-old SHRSP.

Related Experiment Videos

  • Protein levels were compared to age-matched Wistar Kyoto rats (WKY) and younger (15-week-old) SHRSP.
  • Albumin and heat shock protein 70 (HSP70) levels were also assessed as indicators of vascular permeability and cellular injury, respectively.

    • Main Results:

    • A significant decrease in endothelial NOS (eNOS) protein was observed in the cerebral cortex of 31-week-old SHRSP compared to WKY and younger SHRSP.
    • No significant difference was found in the protein amount of neuronal NOS (nNOS).
    • Elevated levels of albumin were detected in the cerebral cortex of 31-week-old SHRSP, suggesting increased vascular permeability. Heat shock protein 70 levels remained unchanged.

    Conclusions:

    • The reduction in eNOS protein, but not nNOS, is strongly associated with the development of stroke in SHRSP.
    • Impaired eNOS function may contribute to the pathophysiology of stroke in this hypertensive model.
    • Further research is warranted to elucidate the precise mechanisms linking eNOS dysfunction to stroke pathogenesis.