The blood brain barrier in renal hypertensive rats.
Spontaneous 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), probably as a result of vessel wall hypertrophy and increased vessel wall to lumen ratio. Hemodynamic studies have indicated that structural adaptation develops early as a response to the increased pressure load in renal hypertensive rats (RHR). In the present study RHR (one 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 cerebral 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 cold 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.
D000808:Angiotensinogen / Q000502:physiology; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D001794:Blood Pressure; D001812:Blood-Brain Barrier / Q000187:drug effects; D001921:Brain / Q000098:blood supply; D002199:Capillary Permeability; D006977:Hypertension, Renal / Q000503:physiopathology*; D051381:Rats; D012711:Serum Albumin, Radio-Iodinated / Q000032:analysis; D014655:Vascular Resistance; D014664:Vasodilation
D012711:Serum Albumin, Radio-Iodinated; D000808:Angiotensinogen; D001640:Bicuculline