Low dietary sodium and exogenous angiotensin II infusion decrease plasma adiponectin concentrations in healthy men

Content: Adiponectin has antiinflammatory 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: Our objective was to 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: Thirty-five healthy male volunteers ( aged 26 +/- 9 yr) were studied after two 7-d periods: one on a low-odium diet ( LS, 50 mmol Na(+) day) and one on a high-sodium diet ( HS, 200 mmol Na(+) per day). At the end of each period, adiponectin was measured, and its response to angiotensin II infusion ( 0.3, 1, and 3 ng/kg center dot min all during 1 h) was determined. Additionally, all subjects received 1 wk treatment of enalapril 20 mg once daily ( angiotensin converting enzyme inhibition) during the HS. Main Outcome Measure: We measured 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 ( 8.31-6.2) mu g/liter; HS baseline, 14.4 ( 11.2 -20.4) mu g/liter; P < 0.05]. All doses of angiotensin II elicited a profound decrease in adiponectin during both conditions [ LS 3 ng/kg center dot min, 7.4 ( 6.3-8.9) mu g/liter; HS 3 ng/kg center dot min, 8.4 ( 7.3-9.9) mu g/liter; both P < 0.001 vs. baseline]. Angiotensin converting enzyme inhibition induced a significant rise in adiponectin [ 16.6 ( 10.6-20.9) mu g/liter, 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 explored further.