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Letter to the Editor

      Romagni et al. [
      • Romagni P.
      • Rossi F.
      • Guerrim L.
      • Quirini C.
      • Santiemma V.
      Aldosterone induces contraction of the resistance arteries in man.
      ] in their recent double blind placebo controlled cross over study, looking at non-genomic vascular effects of aldosterone, found potent constriction (nearly 70%) in the forearm resistance vasculature, in response to intrabrachial aldosterone. This is comparable to the vasoconstriction induced by endothelin in the forearm resistance bed [
      • Strachan F.E.
      • Newby D.E.
      • Sciberras D.G.
      • McCrea J.B.
      • Goldberg M.R.
      • Webb D.J.
      Repeatability of local forearm vasoconstriction to endothelin-1 measured by venous occlusion plethysmography.
      ]. Furthermore, this may have underestimated the magnitude of the effect because it did not appear to have reached a plateau at the end of the 10 min infusion period. In a similar dose response study we observed no changes in forearm blood flow [
      • Gunaruwan P.
      • Schmitt M.
      • Taylor J.
      • Lee L.
      • Struthers A.
      • Frenneaux M.
      Lack of rapid aldosterone effects on forearm resistance vasculature in health.
      ]. Why these conflicting data? We note that there were important differences in the subject characteristics at baseline between the two studies. The basal plasma aldosterone was high in the former (means of 189 and 175 pg/ml) which is within the range for mild to moderate heart failure with ‘aldosterone escape’ [
      • Cicoira M.
      • Zanolla L.
      • Franceschini L.
      • Rossi A.
      • Golia G.
      • Zeni P.
      • et al.
      Relation of aldosterone “escape” despite angiotensin-converting enzyme inhibitor administration to impaired exercise capacity in chronic congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.
      ], whereas in our study the basal plasma aldosterone was 113 pg/ml. The 24 h urine Na+ was also rather elevated (means of 161 and 159 mmol/24 h), reflecting a state of sodium excess, compared with 137.8 mmol/24 h in our study. We speculate that these differences in sodium status may be responsible for the very different findings in the two studies.
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      References

        • Romagni P.
        • Rossi F.
        • Guerrim L.
        • Quirini C.
        • Santiemma V.
        Aldosterone induces contraction of the resistance arteries in man.
        Atherosclerosis. 2003; 166: 345-349
        • Strachan F.E.
        • Newby D.E.
        • Sciberras D.G.
        • McCrea J.B.
        • Goldberg M.R.
        • Webb D.J.
        Repeatability of local forearm vasoconstriction to endothelin-1 measured by venous occlusion plethysmography.
        Br. J. Clin. Pharmacol. 2002; 54: 386-394
        • Gunaruwan P.
        • Schmitt M.
        • Taylor J.
        • Lee L.
        • Struthers A.
        • Frenneaux M.
        Lack of rapid aldosterone effects on forearm resistance vasculature in health.
        J. Renin. Angiotens. Aldoster. Syst. 2002; 3: 123-125
        • Cicoira M.
        • Zanolla L.
        • Franceschini L.
        • Rossi A.
        • Golia G.
        • Zeni P.
        • et al.
        Relation of aldosterone “escape” despite angiotensin-converting enzyme inhibitor administration to impaired exercise capacity in chronic congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.
        Am. J. Cardiol. 2002; 89: 403-407