The present study sought to determine the effects of AV3V lesions on the cardiovascular responses to intravenous HT infusion. Male Wistar rats (300 g) anaesthetized with urethane (1.2 g kg-1, I.V.), after induction with halothane (2 % in 100 O2) had the femoral artery, femoral and jugular vein cannulated for mean arterial pressure (MAP) recording, urethane and HT infusion (3 M NaCl, 0.18 ml (100 g bw)-1, in 60 s), respectively. Renal blood flow (RBF) was recorded by Doppler flowmetry (Transonic) and renal vascular conductance (RVC) was calculated as the ratio RBF (ml min-1)/MAP (mmHg) and expressed as percentage of baseline. At the end of experiments, under deep anaesthesia, rats were perfused transcardially with saline followed by 10 % formalin. The brains were removed, fixed in 10 % formalin, frozen and cut in 40 mm sections, stained with 2 % Neutral Red and analysed by light microscopy to confirm the lesions site. All data are expressed as means ± S.E.M. Two-way repeated measures analysis of variance (ANOVA) followed by Fisher’s protected least-significant differences were used for comparisons. Differences were considered significant at P < 0.05. In sham-operated animals (N = 8), 10 min after HT infusion RBF and RVC increased to 137 ± 10 and 125 ± 7 %, respectively, and at 60 min to 141 ± 10 and 133 ± 10 %. We also observed increases in MAP (peak at 10 min: 11 ± 3 mmHg). Acute AV3V lesion (DC, 2 mA, 25 s, 30 min before infusion, N = 6) abolished MAP increases and the changes in RBF and RVC at 10 min (107 ± 7 and 103 ± 6 %, respectively) and 60 min (107 ± 7 and 106 ± 4 %) after HT infusion. These results demonstrate that the integrity of AV3V region is essential for renal vasodilatation that follows acute changes in the composition of the extracellular fluid compartment.
This work was supported by CNPq-PIBIC, FAPESP, PRONEX and FUNDUNESP.
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