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Low Dietary Sodium and Exogenous Angiotensin II Infusion Decrease Plasma Adiponectin Concentrations in Healthy Men

Department of Internal Medicine, Division of Nephrology (A.T.L., J.A.K., S.J.L.B., G.N.), and Department of Endocrinology (R.P.F.D., B.H.R.W.), University Medical Center Groningen, University of Groningen, 9713 GZ Groningen, The Netherlands; and Department of Internal Medicine (F.B.), Erasmus Medical Center, 3000 CA Rotterdam, The Netherlands

Address all correspondence and requests for reprints to: Titia Lely, Department of Internal Medicine, Division of Nephrology, Hanzeplein 1, 9713 GZ Groningen, The Netherlands. E-mail: a.t.lely{at}int.umcg.nl.

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-sodium diet (LS, 50 mmol Na⁺ per 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·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 (8.3–16.2) µg/liter; HS baseline, 14.4 (11.2–20.4) µg/liter; P < 0.05]. All doses of angiotensin II elicited a profound decrease in adiponectin during both conditions [LS 3 ng/kg·min, 7.4 (6.3–8.9) µg/liter; HS 3 ng/kg·min, 8.4 (7.3–9.9) µg/liter; both P < 0.001 vs. baseline]. Angiotensin converting enzyme inhibition induced a significant rise in adiponectin [16.6 (10.6–20.9) µg/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.