The Blood Brain Barrier in Renal Hypertensive Rats

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Abstract
Spontaneously hypertensive rats (SHR) are less prone to develop a dysfunction of the blood-brain barrier (BBB) when exposed to an abrupt increase in blood pressure than normotensive rats (NR); this may be due to vessel wall hypertrophy and increased vessel wall to lumen ratio. Hemodynamic studies indicated that structural adaptation develops early as a response to the increased pressure load in renal hypertensive rats (RHR). RHR (1 renal artery constricted and the contralateral kidney intact) were subjected to acute hypertension induced by bicuculline, a drug that induces an abrupt increase in blood pressure concomitant with pronounced cerebrl vasodilatation. Protein leakage in the brain, as indicated by Evans blue-albumin and 125IHSA (human serum albumin) extravasation, was not reduced in RHR compared to NR. The cerebrovascular permeability was slightly but significantly (P < 0.01) increased in RHR even in the absence of further blood pressure manipulation. No neurological symptoms were observed in conscious RHR when the BBB dysfunction was aggravated by hypercapnia. The increased cerebrovascular permeability in RHR could be due to a lower degree of structural adaptation in RHR compared to SHR and/or to some permeability-increasing humoral factor in renal hypertension.