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 cardiovascular adjustments to volume expansion (VE) with 4% Ficoll (1% body weight, 1.4 mL/min) was studied in urethane-anesthetized rats. In sham-lesioned animals, VE produced a transitory (</=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, respectively, 10 and 40 minutes after VE) and hindlimb vascular (157+/-19% and 153+/-9% of baseline) conductance. After AV3V lesions, VE induced a sustained increase in mean arterial pressure. Although renal blood flow increased in response to VE, renal vascular conductance was unaffected, indicating that renal 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 the AV3V region is essential for the renal vasodilation induced by VE.