Published online before print May 14, 2007, doi: 10.1161/HYPERTENSIONAHA.107.088955
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(Hypertension. 2007;50:82.)
© 2007 American Heart Association, Inc.
Original Articles |
Influence of Acute and Chronic Mineralocorticoid Excess on Endothelial Function in Healthy Men
From the Clinic of Cardiology, Department of Internal Medicine (F.N., R.S., A.B., H.P.B.-L.R.), University Hospital Basel, Switzerland; the Division of Cardiology, Department of Internal Medicine (B.J.), Kantonsspital Aarau, Switzerland; Actelion Pharmaceuticals (C.B.), Allschwil, Switzerland; and HerzGefässZentrum Klinik Im Park Zürich (W.K.), Switzerland.
Correspondence to Hans Peter Brunner-La Rocca, MD, Clinic of Cardiology, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland. E-mail hbrunner{at}uhbs.ch
Aldosterone has rapid nongenomic effects in the human vasculature. However, data are not uniform and little is known about chronic effects of aldosterone. Therefore, we investigated acute and chronic effects of elevated aldosterone levels on endothelial function in the forearm vasculature of healthy men. In a first crossover study, the effects of arterial aldosterone infusion in ascending doses (3.3 to 55 pmol/min per 1000 mL forearm volume) on forearm blood flow were investigated in 8 healthy men (26±2 years). In a second study, endothelium-dependent (acetylcholine; 0.08, 0.275, and 2.75 µmol/min per 1000 mL) and endothelium-independent (sodium nitroprusside 0.02 µmol/min per 1000 mL) vasodilation and basal nitric oxide formation (forearm blood flow response to blockade by NG-monomethyl-L-arginine 8 µmol/min per 1000 mL) were tested in 10 healthy men (age 30±5 years) at baseline, during infusion of 55 pmol/1000 mL per min aldosterone (acute effects), and after 0.3 mg/d oral fludrocortisone for 2 weeks (chronic effects) on separate days. Forearm blood flow was assessed by venous occlusion plethysmography. No change in forearm blood flow was seen with aldosterone infusion alone. Acute coinfusion of aldosterone increased vasodilation to sodium nitroprusside by 93% (P<0.01) and to acetylcholine by 60% (P=0.14). Response to NG-monomethyl-L-arginine did not change. After 2 weeks of oral fludrocortisone, response to acetylcholine was enhanced by 72% compared with baseline (P=0.03). Additionally, response to NG-monomethyl-L-arginine was enhanced by 80% compared with baseline (P=0.05). Aldosterone acutely enhances vasodilation to exogenous nitric oxide whereas mineralocorticoid excess for 2 weeks enhances basal nitric oxide bioactivity and improves endothelium dependent, nitric oxide–mediated vasodilation in the forearm vasculature of healthy men.
Key Words: aldosterone • endothelial function • mineralocorticoid excess • forearm vasculature • nitric oxide
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