Cerebroventricular dilation in spontaneously hypertensive rats (SHRs) is not attenuated by reduction of blood pressure.
In previous studies, we found that spontaneously hypertensive rats (Okamoto-Aoki SHRs) suffer progressive postnatal dilation of the brain ventricles. In the present study we examined intracerebroventricular pressure and blood pressure as possible mechanisms of ventricular dilation in SHRs. We found that intracerebroventricular pressure was not elevated in SHRs. The role of blood pressure was examined in SHRs treated chronically with the antihypertensive drug, captopril, beginning in utero, and in renal hypertensive Sprague-Dawley rats (SDs). Although our experimental treatments produced significant changes in mean arterial pressures, they did not alter brain ventricular size: SDs with experimental hypertension had normal-sized brain ventricles and SHRs with pharmacologically reduced blood pressure had enlarged ventricles. These results suggest that neither increased intraventricular pressure nor high blood pressure is the sole cause of hydrocephalus in SHRs.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002216:Captopril / Q000494:pharmacology*; D002552:Cerebral Ventricles / Q000473:pathology*; D004108:Dilatation, Pathologic; D005260:Female; D006973:Hypertension / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains
D002216:Captopril