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Cerebrovascular Permeability in Mechanically Induced Hypertension

Published online by Cambridge University Press:  18 September 2015

Sukriti Nag ,
David M. Robertson  and
Henry B. Dinsdale
Sukriti Nag*
Affiliation:
Departments of Pathology and Medicine, Queen’s University and Kingston General Hospital, Kingston, Ontario, Canada
David M. Robertson
Affiliation:
Departments of Pathology and Medicine, Queen’s University and Kingston General Hospital, Kingston, Ontario, Canada
Henry B. Dinsdale
Affiliation:
Departments of Pathology and Medicine, Queen’s University and Kingston General Hospital, Kingston, Ontario, Canada
*
Department of Pathology, Queen’s University, Kingston, Ontario, Canada K7L 3N6
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Our previous studies of cerebrovascular permeability in angiotensin-induced acute hypertension demonstrated that the principal mechanism resulting in increased permeability is enhanced pinositose. In order to exclude the possibility that the enhanced pinositose was a direct effect of exogenous angiotensin, cerebrovascular permeability alterations were studied in nonpharmacologically induced acute hypertension.

Rats receiving horseradish peroxidase (HRP) intravenously, were sacrificed 2½ minutes after the onset of hypertension induced by placing a clip on the abdominal aorta. These animals showed the same pattern of permeability alterations as had been observed previously in animals with angiotensin-induced acute hypertension. Focal segments of penetrating arterioles in the temporal and parietal cortex showed increased permeability to HRP. Permeable vessels showed increased numbers of pinocytotic vesicles and the interendothelial junctions revealed no alterations. Enhanced pinocytosis appears to be the principal mechanism resulting in increased cerebrovascular permeability in this model as well suggesting that the alterations of cerebrovascular permeability observed previously in angio-tensin-induced acute hypertension occur due to the hypertensive state and are not a direct drug effect of exogenous angiotensin.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 8 , Issue 3 , August 1981 , pp. 215 - 220
Copyright
Copyright © Canadian Neurological Sciences Federation 1981

References

REFERENCES

Beggs, J.L., Waggener, J.D. (1979). The acute microvascular responses to spinal cord injury. Adv. Neurol. 22 eds, Thompson, R.A. and Green, J.R., Raven Press, New York, 179–189.Google Scholar
Brightman, M.W., Klatzo, I., Olsson, Y., Reese, T.S. (1970). The blood-brain barrier to proteins under normal and pathological conditions. J. Neurol. Sci. 10: 215–239.CrossRefGoogle ScholarPubMed
Hanker, J.S., Yates, P.E., Metz, C.B., Rustioni, A. (1977). A new specific, sensitive and non-carcinogenic reagent for the demonstration of horseradish peroxidase. Histochem. J. 9: 789–792.CrossRefGoogle ScholarPubMed
Hansson, H-A, Johansson, B., Blomstrand, C. (1975). Ultrastructural studies on cerebrovascular permeability in acute hypertension. Acta Neuropathol. (Berl.) 32: 187–198.CrossRefGoogle ScholarPubMed
Johansson, B., Linder, L-E. (1974). Blood-brain barrier dysfunction in acute arterial hypertension induced by clamping of the thoracic aorta. Acta Neurol. Scand. 50: 360–365.CrossRefGoogle ScholarPubMed
Karnovsky, M.J. (1967). The ultrastructural basis of capillary permeability studied with peroxidase as a tracer. J. Cell. Biol. 35: 213–236.CrossRefGoogle ScholarPubMed
Lossinsky, A.S., Garcia, J.H., Iwanowski, L., Lightfoote, W.E. Jr. (1979). New ultrastructural evidence for a protein transport system in endothelial cells of gerbil brains. Acta Neuropathol. (Berl.) 47: 105–110.CrossRefGoogle ScholarPubMed
Meyer, J.S., Waltz, A.G., Gotoh, F. (1960). Pathogenesis of cerebral vasospasm in hypertensive encephalopathy. Neurology 10: 735–744.CrossRefGoogle Scholar
Nag, S., Robertson, D.M., Dinsdale, H.B. (1977). Cerebral cortical changes in acute experimental hypertension. An ultrastructural study. Lab. Invest. 36: 150–161.Google ScholarPubMed
Nag, S., Robertson, D.M., Dinsdale, H.B. (1979). Quantitative estimate of pinocytosis in experimental acute hypertension. Acta Neuropathol. (Berl.) 46: 107–116.CrossRefGoogle ScholarPubMed
Nag, S., Robertson, D.M., Dinsdale, H.B. (1980). Morphological changes in spontaneously hypertensive rats. Acta Neuropathol. (Berl.) 52: 27–34.CrossRefGoogle ScholarPubMed
Nagy, Z., Mathieson, G., Hüttner, I. (1979). Blood-brain barrier opening to horseradish peroxidase in acute arterial hypertension. Acta Neuropathol. (Berl.) 48: 45–53.CrossRefGoogle ScholarPubMed
Petito, C.K., Levy, D.E. (1980). The importance of cerebral arterioles in alterations of the blood-brain barrier. Lab Invest. 43: 262–268.Google ScholarPubMed
Sen, S., Smeby, R.R., Bumpus, F.M. (1972). Renin in rats with spontaneous hypertension. Circ. Res. 31: 876–880.CrossRefGoogle ScholarPubMed
Sokabe, H. (1965). Renin-angiotensin system in the spontaneously hypertensive rat. Nature 205: 90.Google Scholar
Westergaard, E., Van Deurs, B., Brøndsted, H.E. (1977). Increased vesicular transfer of horseradish peroxidase across cerebral endothelium, evoked by acute hypertension. Acta Neuropathol. (Berl.) 37: 141–152.CrossRefGoogle ScholarPubMed