Content Adiponectin has anti-inflammatory and vascular protective effects, and may improve insulin sensitivity. Animal data suggest a role of the renin-angiotensin aldosterone system (RAAS) in the regulation of adiponectin.

Objective Investigate the role of the RAAS in regulation of adiponectin in humans in vivo. To this purpose we studied the effects of physiological (change in sodium status) and pharmacological modulation of RAAS activity (angiotensin II infusion and enalapril treatment) on plasma adiponectin.

Design, setting and patients 35 healthy male volunteers (aged 26 ± 9 years) were studied after two 7 day periods; one on low sodium (LS: 50 mmol Na⁺/day) and one on high sodium (HS: 200 mmol Na⁺/day). At the end of each period, adiponectin was measured and its response to angiotensin II infusion (0.3, 1 and 3 ng/kg/hr all during 1 hour) was determined. Additionally, all subjects received administrated to one week treatment of enalapril 20 mg once daily (ACEi) during HS.

Main Outcome measure Plasma adiponectin concentrations during LS and HS and in response to angiotensin II infusion.

Results The suppression of the RAAS by HS elicited a significant rise in adiponectin (LS baseline 11.9 (8.3-16.2) ug/L); HS baseline 14.4 (11.2-20.4) ug/L, p<0.05). All dosages angiotensin II elicited a profound decrease in adiponectin during both conditions (LS 3 ng/kg/hr 7.4 (6.3-8.9) ug/L, HS 3 ng/kg/hr 8.4 (7.3-9.9) ug/L both p<0.001 vs. baseline). ACEi induced a significant rise in adiponectin (16.6 (10.6-20.9) ug/L, p<0.05 vs HS).

Conclusion Physiological and pharmacological modulation of RAAS affects plasma adiponectin with lower concentrations during the high angiotensin II conditions. The therapeutic potential of RAAS-blockade as a tool to correct hypoadiponectinemia should be further explored.