Prevention of the development of renal hypertension by anteroventral third ventricular tissue lesions.

Several reports have suggested that a central action of the renin-angiotensin system plays a role in the development of renal hypertension. Based on the identification of the anteroventral thrid ventricle (AV3V) as a site of central angiotensin dipsogenic and pressor mechanisms, the present study examined the effect of electrolytic lesions in the AV3V region on the development of renal hypertension in rats. Lesioning alone produced a temporary but profound adipsia and, in one-half of the rats, a substantial transient elevation in arterial pressure. After lesioned rats had recovered normal drinking and blood pressure, unilateral nephrectomy with figure-of-eight wrapping of the remaining kidney failed to produce the hypertension and increased drinking observed after renal wrapping in shamlesioned rats. The possibility that the failure of lesioned rats to increase water intake after wrapping prevents hypertension development was ruled out by experiments demonstrating that normal rats exhibited identical rises in arterial pressure after wrapping regardless of whether or not they were allowed to increase water intake. The fact that unanesthetized lesioned rats exhibit attenuated drinking and pressor responses to systemically administered angiotensin suggests this mechanism as a possible explanation for the failure of AVV-lesioned rats to increase drinking and blood pressure after renal wrapping.