Effects of acute AV3V lesions on renal and hindlimb vasodilation induced by volume expansion

The role of the anteroventral third ventricle (AV3V) region in the cardiova scular adjustments to volume expansion (VE) with 4% Ficoll (1% body weight, 1.4 mL/min) was studied in urethane-anesthetized rats. In sham-lesioned an imals, VE produced a transitory (less than or equal to 20 minutes) increase in mean arterial pressure, which peaked at 10 minutes (10+/-3 mm Hg), and sustained increases of renal (123+/-10% and 127+/-6% of baseline, respectiv ely, 10 and 40 minutes after VE) and hindlimb vascular (157+/-19% and 153+/ -9% of baseline) conductance. After AV3V lesions, VE induced a sustained in crease in mean arterial pressure. Although renal blood flow increased in re sponse to VE, renal vascular conductance was unaffected, indicating that re nal vasodilation was abolished. On the other hand, after AV3V lesions, the increases in hindlimb blood flow and vascular conductance were higher than those observed in sham-lesioned rats. Results obtained demonstrated that th e AV3V region is essential for the renal vasodilation induced by VE.