Cerebroventricular Dilation in Spontaneously Hypertensive Rats (SHRs) Is Not Attenuated by Reduction of Blood Pressure
In a previous study, we noted that spontaneously hypertensive rats (SHRs) suffer postnatal dilation of the brain ventricular spaces and concomitant loss of brain tissue (S. Ritter and T.T. Dinh, Brain Research 370: 327–332, 1986). In that study, cross-sectional areas of the forebrain ventricles were measured from coronal sections in SHRs 4, 8, 12, 16, 21 and 56 weeks of age and in age-matched Wistar-Kyoto (WKY) and Sprague-Dawley (SD) normotensive rats. Progressive ventricular dilation and associated attrition of brain tissue was observed in SHRs of both sexes after 4 weeks of age, and was present in animals obtained from two different suppliers. In the present study we examined two possible mechanisms of ventricular dilation in the SHR. First, we measured intracerebroventricular pressure by lateral ventricular cannulation but found that pressures did not differ between SHRs and WKYs. Second, we examined the effect of blood pressure on ventricular size. Hypertension was attenuated in SHRs by chronic treatment with the antihypertensive drug, Captopril, beginning in utero and continuing throughout life. In addition, genetically normotensive SDs were made hypertensive by constriction of the renal artery at 4 weeks of age. Blood pressures were monitored non-invasively throughout the experiment. Captopriltreated rats were sacrificed at 16 weeks and renal hypertensive (“clamped”) rats at 22 weeks of age.