Abstract P249: Central Nervous System Control of Plasma Aldosterone and Endogenous Ouabain in Angiotensin II-Salt Hypertension

High salt intake markedly enhances hypertension induced by Ang II. We evaluated peripheral mechanisms which may amplify central mechanisms activated by Ang II-salt. In the 1 st exp, Wistar rats were sc infused with Ang II at low dose of 150 ng/kg/min together with 2% high salt diet for 14 days. In the 2 nd exp, MR blockers (eplerenone, spironolactone), ENaC blocker (benzamil), AT 1 R blocker (losartan) or vehicles (Veh) were icv infused combined with Ang II-salt. BP was recorded by telemetry. Plasma corticosterone (Cor), aldosterone (aldo) and endogenous ouabain (EO) were measured by RIA. Gene expression was assessed by real-time qPCR. Ang II alone caused a small increase in MAP (112±1 vs. 99±1 mmHg), but BP was markedly increased by Ang II-salt (152±4 mmHg, P1 R mRNA expression. Central blockades significantly (p1 R mRNA but markedly decreased Ang II-salt induced CYP11B2 expression in the adrenal cortex. Together, these results suggest that in Ang II-salt hypertension, Ang II-AT 1 R signaling and MR-ENaC pathway in the brain increase plasma aldo and EO, which may amplify BP responses to central mechanisms and contribute to severe hypertension by Ang II-salt vs Ang II alone.