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.

No rarefaction of cerebral arterioles in hypertensive rats.

A reduction in the density of small arterioles (rarefaction) has been reported in several vascular beds of the spontaneously hypertensive rat (SHR). There have been conflicting reports on the existence of rarefaction in the pial vasculature of SHR. In this study, we determined whether there was rarefaction of pial arterioles in several models of hypertension. We studied SHR; two-kidney, one-clip Goldblatt hypertensive rats; deoxycorticosterone-salt hypertensive rats; and Dahl salt-sensitive rats fed high salt diet. The two groups of normotensive controls were Wistar--Kyoto rats and Dahl salt-sensitive rats fed low salt diet. The duration of hypertension was about 2 months. Density of first-, second-, third-, and fourth-order arterioles was determined by counting the number of vessels from enlarge photographs. We also measured the lengths of segments of the arterioles. We did not observe any evidence of rarefaction of arterioles in the pial vasculature in any of the hypertensive groups of rats. We conclude that (i) rarefaction of arterioles does not occur in the pial microvasculature after approximately 2 months of hypertension and (ii) rarefaction of pial arterioles does not account for abnormalities in the cerebral circulation of hypertensive rats such as protection of the blood-brain barrier or changes in autoregulation of cerebral blood flow.

Hypertension and cerebral arteries: relationship to disruption of the blood-brain barrier.

This study was performed to determine whether structural changes in cerebral arterioles could account for differences in susceptibility of the blood-brain barrier to acute hypertensive disruption between hypertensive and normotensive animals. We studied spontaneously hypertensive rats (SHR), 3 other models of hypertension and their normotensive controls. The age and duration of hypertension of the rats were matched to an earlier study showing that protection of the blood-brain barrier was usually found in rats with chronic hypertension. We measured the dimensions of fixed pial arterioles and minimal cerebrovascular resistance produced by bicuculline. Minimal cerebrovascular resistance was not different between the groups of animals. There were no differences in the area of the media of pial arterioles between any of the groups. In addition, we examined the possibility that sympathetic nerves might affect cerebrovascular resistance during bicuculline in SHR. The presence of sympathetic nerves in SHR, but not WKY, reduced the degree of cerebral vascular dilation during bicuculline. From these data we conclude that 1) structural changes in cerebral vessels do not account for protection of the blood-brain barrier in rats with a moderate duration of hypertension and 2) sympathetic nerves may have an exaggerated effect on cerebral vessels of SHR.

Effect of chronic hypertension on acute hypertensive disruption of the blood-brain barrier in rats.

The effect of chronic hypertension on acute hypertensive disruption of the blood-brain barrier has been studied in only two models of hypertension, with inconsistent results. The purpose of this study was to reinvestigate whether chronic hypertension has a consistent effect on acute hypertensive disruption of the blood-brain barrier and to determine whether one of the previously studied models has an unusual response to chronic hypertension. We studied four rat models of chronic hypertension: spontaneously hypertensive rats (SHR), two-kidney, 1 clip Goldblatt rats (2K1C), rats treated with deoxycorticosterone acetate (DOCA) and NaCl, Dahl salt-sensitive rats fed a high salt diet, and two groups of normotensive controls: Wistar-Kyoto rats (WKY) and Dahl salt-sensitive rats fed a low salt diet. We caused acute hypertension in some rats with the use of bicuculline (1.2 mg/kg) and aortic occlusion. Rats without acute hypertension served as controls. Blood-brain barrier disruption was quantitated using the brain/blood ratio of 125I-labeled albumin. Acute hypertensive disruption was less in SHR, rats treated with DOCA-NaCl, and Dahl salt-sensitive rats fed a high salt diet, but not in 2K1C rats, as compared with normotensive controls. Acute hypertensive disruption was greater in Dahl salt-sensitive rats fed a low salt diet than in WKY. A series of control WKY, SHR, rats treated with DOCA-NaCl, 2K1C rats, and Dahl salt-sensitive rats fed low or high salt diets, but not subjected to acute hypertension, were also studied. Brain/blood 125I-albumin ratios were significantly less in these control rats not subjected to acute hypertension than in rats subjected to acute hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)