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Presence of Transendothelial Channels in Cerebral Endothelium in Chronic Hypertension

Part of the Acta Neurochirurgica book series (NEUROCHIRURGICA, volume 51)

Summary

In this model hypertension developed as early as 1 wk. post-surgery and was associated with reduction in Ca2+-ATPase activity in cerebral vessels indicating that abnormalities in ionic calcium in vessel walls occur early in the evolution of hypertension. This study supports previous observations1 that cerebral cortical arterioles develop increased permeability to endogenous plasma proteins in chronic hypertension. The principal mechanism resulting in this increased permeability is enhanced pinocytosis. Ca2+-ATPase localisation in endothelial pinocytotic vesicles helped to localise transendothelial channels in occasional vessels of hypertensive rats.

The latter findings reinforce the concept that in pathologic states associated with cerebral oedema, pinocytotic vesicles fuse to form transendothelial channels which transport plasma proteins into brain.

Keywords

Evans Blue Chronic Hypertension Outer Plasma Membrane Pinocytotic Vesicle Arteriolar Wall 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Nag S (1984) Cerebral changes in chronic hypertension: combined permeability and immunohistochemical studies. Acta Neuropathol (Berl) 62: 178–184CrossRefGoogle Scholar
  2. 2.
    Nag S (1985) Ultrastructural localisation of monosaccharide residues on cerebral endothelium. Lab Invest 5: 553–558Google Scholar
  3. 3.
    Nag S (1988) Localisation of calcium-activated adenosine-triphosphatase (Ca’-ATPase) in intracerebral arterioles in acute hypertension. Acta Neuropathol (Berl) 75: 547–553CrossRefGoogle Scholar

Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • S. Nag
    • 1
  1. 1.Department of Pathology (Neuropathology)Queen’s University and Kingston General HospitalKingstonCanada

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