Influence of forebrain periventricular lesions on the development of renal hypertension in rabbits.

Ablation of tissue surrounding the anteroventral third cerebral ventricle (AV3V) has been demonstrated to prevent and reverse renal hypertension in the rat. The contribution of this brain area to the maintenance of hypertension in other species has not been examined. In the present investigation, an attempt was made to produce two-kidney, one clip renal hypertension in rabbits with histologically and functionally defined AV3V destruction. Electrolytic lesion of the AV3V in rabbits produced effects closely resembling those previously seen in rats: increased plasma volume and plasma sodium, temporary adipsia, no change in resting arterial pressure or heart rate, and significant attenuation of pressor responsiveness to angiotensin II (AII) delivered intracranially. However, the increase in arterial pressure observed over a 4-week period following the application of a 0.5 mm silver clip to the left renal artery (opposite kidney intact) was identical in 12 AV3V-lesioned and 12 sham-operated rabbits. Hypertension development was not accompanied by significant sodium retention, water retention, or plasma/extracellular fluid volume expansion in either group of rabbits. Pressor responses to intravenous infusions of AII and norepinephrine were identical in sham and AV3V-X rabbits. Thus, destruction of the AV3V, and the attendant reduction in the central pressor action of AII, does not alter the pattern of development of two-kidney, one clip renal hypertension in the rabbit. The contrasting results in rats and rabbits could be explained by the differing contribution of the area postrema to the pressor action of AII in the two species.