Pial venous pressure and acute hypertensive disruption of the blood-brain barrier in spontaneous and renal hypertension.
The purpose of this study was to determine whether changes in pial venous pressure during acute hypertension account for altered acute hypertensive disruption of the blood-brain barrier in chronic hypertension. We studied 13 normotensive WKY rats, 7 spontaneously hypertensive rats (SHR), and 9 two-kidney, one-clip renal hypertensive rats of the same age. Pial venous pressure (servonull technique) and clearance of fluorescein-labeled dextran from pial vessels (as an estimate of permeability of the blood-brain barrier) were measured before and during acute hypertension produced by i.v. infusion of phenylephrine. Experiments were performed in anesthetized rats (50 mg/kg sodium pentobarbital i.p.). Blood and artificial cerebrospinal fluid pO2, pCO2 and pH were within normal ranges throughout the experiment. The change, time to peak and peak pial venous pressures were the same in all groups. The peak arterial pressure after phenylephrine was greater in the hypertensive rats compared to WKY rats. The time to peak mean arterial pressure was the same in all groups of rats. Clearance of FITC dextran was the same in WKY versus renal hypertensive rats, but less in SHR versus WKY rats (P less than 0.05 by analysis of variance). We conclude that something other than an attenuation of the increase in pial venous pressure protects the blood-brain barrier of SHR against acute hypertensive disruption.
Werber
A H
AH
Department of Pharmacology and Toxicology, Albany Medical College, NY 12208.
Fitch-Burke
M C
MC
D000818:Animals; D001812:Blood-Brain Barrier; D002550:Cerebral Veins / Q000503:physiopathology*; D006977:Hypertension, Renal / Q000503:physiopathology*; D007427:Intracranial Pressure; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains