Mechanisms of protection of the blood-brain barrier during acute hypertension in chronically hypertensive rats

William G. Mayhan, Frank M. Faraci, Donald D. Heistad

Research output: Contribution to journalArticle

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Abstract

Spontaneously hypertensive rats are less susceptible than normotensive rats to disruption of the blood-brain barrier during acute hypertension. The purpose of this study was to examine mechanisms that protect the blood-brain barrier from disruption in chronically hypertensive rats during acute hypertension. Normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were studied using intravital fluorescent microscopy and fluoresceinlabeled dextran. Disruption of the blood-brain barrier was characterized by the appearance of micro vascular leaky sites and quantitated by the clearance of fluorescein-labeled dextran. We measured pressure (servo null) in pial arterioles and venules 40 to 60 jam in diameter. In WKY, acute, phenylephrine-induced hypertension increased pial arteriolar pressure by 47 ± 7 mm Hg (mean ± SE) and pial venous pressure by 20 ± 2 mm Hg. Leaky sites increased from 0 to 28 ± 2. In SHRSP, acute hypertension increased pial arteriolar pressure 44 ± 8 mm Hg, but pial venous pressure increased only 6 ± 1 mm Hg and leaky sites increased from 0 to only 6 ± 1. All leaky sites were venular. In another group of WKY and SHRSP, we increased pial venous pressure passively with a neck cuff. In WKY, venous pressure increased by 22 ± 2 mm Hg, and leaky sites increased from 0 to 23 ± 2. In SHRSP, venous pressure increased by 19 ± 1 mm Hg, and leaky sites increased from 0 to 24 ± 2. Thus, when venous pressure is increased to the same level in WKY and SHRSP, disruption of the blood-brain barrier is similar. We conclude that 1) protection of the blood-brain barrier during acute hypertension in SHRSP is related to attenuation of increases in pial venous pressure, not pial arteriolar pressure, and 2) the blood-brain barrier in venules of SHRSP probably is not inherently resistant to disruption.

Original languageEnglish (US)
Pages (from-to)III-101-III-105
JournalHypertension
Volume9
Issue number6, Part 2
StatePublished - Jun 1987

Fingerprint

Venous Pressure
Blood-Brain Barrier
Inbred WKY Rats
Hypertension
Pressure
Venules
Inbred SHR Rats
Arterioles
Phenylephrine
Dextrans
Blood Vessels
Neck
Stroke

Keywords

  • Fluorescein isothiocynate-labeled dextran
  • Stroke-prone spontaneously hypertensive rats
  • Venous pressure

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Mechanisms of protection of the blood-brain barrier during acute hypertension in chronically hypertensive rats. / Mayhan, William G.; Faraci, Frank M.; Heistad, Donald D.

In: Hypertension, Vol. 9, No. 6, Part 2, 06.1987, p. III-101-III-105.

Research output: Contribution to journalArticle

Mayhan, William G. ; Faraci, Frank M. ; Heistad, Donald D. / Mechanisms of protection of the blood-brain barrier during acute hypertension in chronically hypertensive rats. In: Hypertension. 1987 ; Vol. 9, No. 6, Part 2. pp. III-101-III-105.
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AB - Spontaneously hypertensive rats are less susceptible than normotensive rats to disruption of the blood-brain barrier during acute hypertension. The purpose of this study was to examine mechanisms that protect the blood-brain barrier from disruption in chronically hypertensive rats during acute hypertension. Normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were studied using intravital fluorescent microscopy and fluoresceinlabeled dextran. Disruption of the blood-brain barrier was characterized by the appearance of micro vascular leaky sites and quantitated by the clearance of fluorescein-labeled dextran. We measured pressure (servo null) in pial arterioles and venules 40 to 60 jam in diameter. In WKY, acute, phenylephrine-induced hypertension increased pial arteriolar pressure by 47 ± 7 mm Hg (mean ± SE) and pial venous pressure by 20 ± 2 mm Hg. Leaky sites increased from 0 to 28 ± 2. In SHRSP, acute hypertension increased pial arteriolar pressure 44 ± 8 mm Hg, but pial venous pressure increased only 6 ± 1 mm Hg and leaky sites increased from 0 to only 6 ± 1. All leaky sites were venular. In another group of WKY and SHRSP, we increased pial venous pressure passively with a neck cuff. In WKY, venous pressure increased by 22 ± 2 mm Hg, and leaky sites increased from 0 to 23 ± 2. In SHRSP, venous pressure increased by 19 ± 1 mm Hg, and leaky sites increased from 0 to 24 ± 2. Thus, when venous pressure is increased to the same level in WKY and SHRSP, disruption of the blood-brain barrier is similar. We conclude that 1) protection of the blood-brain barrier during acute hypertension in SHRSP is related to attenuation of increases in pial venous pressure, not pial arteriolar pressure, and 2) the blood-brain barrier in venules of SHRSP probably is not inherently resistant to disruption.

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