Role for peripheral V1 receptor activation in the pressor and renal sympathoexcitatory responses to ICV angiotensin II (ANGII)

ANGII infused ICV in rats on a normal Na + (NNa + ) diet leads to a pressor response and a fall in renal sympathetic nerve activity (RSNA) while rats fed a high Na + (HNa + ) diet also express a later rise in RSNA. This study investigated the impact of peripheral V 1 receptor blockade (V 1 B) on these responses. Male Wistar rats fed a NNa + (0.3% Na + ) or HNa + (3.0%, Na + ) diet for 6 weeks were anaesthetized, cannulae inserted into the femoral artery/vein and right ICV and RSNA recorded from the left kidney. Blood pressure (BP) and RSNA were measured after ICV ANGII (50–100ng in 2μL; NNa + n=7–10) and during V 1 blockade (V 1 B, Manning compound, 10μg/0.2mL IV; n=6). Data (mean±SE) were compared by ANOVA. P<0.05 indicated significance. Basal BP (mmHg) was similar between groups (ANGII: NNa + 89±4 , HNa + 95±4; ANGII + V 1 B: NNa + 89±4 , HNa + 84±4). The 30 min area under the curve (AUC) BP response (ΔmmHg∗min) was less during V 1 B in NNa + (ANGII: 232±47 vs ANGII+ V 1 B: 60±29, P<0.05) and HNa + (ANGII: 237±66 vs ANGII+ V 1 B: 73±13, P<0.05). RSNA fell immediately after ICV ANGII in NNa + (ANGII: 94±3%, ANGII+ V 1 B: 94±2, P<0.05) and HNa + (ANGII: 84±6%, ANGII + V 1 : 91±3%, P<0.05 vs baseline) with no effect of V 1 B. The rise in RSNA in the HNa + rats 30 min after ICV ANGII was not present during V 1 B (ANGII:112±2%, ANGII + V 1 B: 96±6%, P<0.05). The results suggest that V 1 receptor activation contributes to the BP and long term rise in RSNA to ICV ANGII. Funding: HRB RP/2004/17.