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Related Experiment Videos

Kinins induce abnormal vascular reactivity.

E F Ellis1, S A Holt, E P Wei

  • 1Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.

The American Journal of Physiology
|August 1, 1988
PubMed
Summary
This summary is machine-generated.

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Kinins initiate cerebrovascular abnormalities after neural trauma by stimulating prostaglandin H synthase, leading to free radical-mediated injury. Blocking kinin receptors prevents these damaging effects, suggesting kinins are key mediators of vascular damage.

Area of Science:

  • Neuroscience
  • Vascular Biology
  • Biochemistry

Background:

  • Neural trauma and hypertension induce superoxide radicals and cerebrovascular damage.
  • Prostaglandin H synthase (PGH synthase) activity and subsequent oxygen radical formation are implicated in this vascular injury.
  • Free radical scavengers and PGH synthase inhibitors prevent these abnormalities.

Purpose of the Study:

  • To investigate the role of kinins in initiating cerebrovascular abnormalities following neural trauma in cats.
  • To determine if kinins stimulate arachidonate metabolism and superoxide anion production in cerebral arterioles.

Main Methods:

  • Comparison of in vivo pial arteriole diameter and reactivity between untreated and kinin receptor antagonist-treated feline cerebral cortices.
  • Topical application of a specific competitive kinin receptor antagonist.

Related Experiment Videos

  • Induction of fluid percussion neural trauma.

    • Main Results:

    • Untreated arterioles showed dilation and loss of reactivity to CO2 after trauma.
    • Arterioles pretreated with the kinin antagonist exhibited reduced dilation and maintained normal reactivity to CO2.
    • These findings indicate a specific kinin receptor mediates PGH synthase-dependent, free radical-induced cerebrovascular injury.

    Conclusions:

    • Kinin receptor stimulation triggers PGH synthase-dependent, free radical-mediated cerebrovascular injury.
    • The kallikrein-kinin system, through kinins, may be a significant mediator of systemic vascular injury and altered vascular reactivity.