gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Rapid, nongenomic aldosterone effects are enhanced in essential hypertensives

Schnelle, nicht-genomische Aldosteron-Effekte sind bei Hypertonikern verstärkt

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker B.M.W. Schmidt - Universität Erlangen-Nürnberg (Nürnberg, D)
  • A. Rastätter - Universität Erlangen-Nürnberg (Nürnberg, D)
  • T. Schwarz - Universität Erlangen-Nürnberg (Nürnberg, D)
  • M.P. Schneider - Universität Erlangen-Nürnberg (Nürnberg, D)
  • S. Oehmer - Universität Erlangen-Nürnberg (Nürnberg, D)
  • R.E. Schmieder - Universität Erlangen-Nürnberg (Nürnberg, D)

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochV12

The electronic version of this article is the complete one and can be found online at:

Published: November 11, 2004

© 2004 Schmidt et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Rapid nongenomic aldosterone effects have been proposed to be important in hypertension in addition to genomic aldosterone effects. We have shown a vasoconstricitve response to intravenous aldosterone infusion in healthy male volunteers, which occurred within 30 minutes. Recently, we described that in the human forearm aldosterone increases the vasoconstrictive response to phenylephrine and L-NMMA within 20 minutes after start of an intraarterial aldosterone infusion. Based on these data we hypothesized that aldosterone might be a stronger vasoconstrictor in hypertensives than in normotensives.

To address this issue we examined 12 normotensive and 12 mildly hypertensive young males. In hypertensives secondary hypertension was excluded by clinical and laboratory measures. All hypertensives were previously and currently untreated and showed no hypertensive target organ damage.

We infused aldosterone (Clinalfa, Läufelingen, Switzerland) for 60 minutes (0,1 mg as bolus and 3 µg/min as continuous infusion). Cardiovascular parameters were measured using the Task Force Monitor device (CNSystems, Graz, Austria). Primary endpoint of our study was the change in total peripheral resistance index (TPRI) during the aldosterone infusion. Furthermore we evaluated stroke volume index (SVI), cardiac index (CI) and mean arterial blood pressure (MAP). For statistical comparison t-test and multifactorial (timepoint, group) ANOVA were used were applicable.

At baseline, hypertensives showed higher blood pressure (144 ± 11 / 89 ± 11 vs. 128 ± 8 / 79 ± 8, p < 0.05) and higher heart rate (71 ± 12 vs. 66 ± 12, p < 0.01). There were no differences between both groups regarding age (29.3 ± 6,5 vs. 28.4 ± 5.9 years) and BMI (25,4 ± 3.2 vs. 24.0 ± 3.9 kg/m2). TPRI was slightly higher in hypertensives (44.2 ± 9.8 vs. 38.3 ± 7.6 mmHg*L-1*min, n.s.), SVI was lower (35 ± 7 vs. 44 ± 10 ml/ m2, p < 0.05), and CI was identical (2.3 ± 0.4 vs. 2.3 ± 0.5 L/min*m2).

During aldosterone infusion TPRI increased in both groups. The increase was more pronounced in hypertensives reaching 2.4 ± 2.6 mmHg*L-1*min vs. 0.5 ± 1.2 mmHg*L-1*min after 15 minutes (p<0.05). Looking at the mean change over the whole time period of 60 minutes the difference was also statistically significant (2.1 ± 4.8 vs. 0.3 ± 2.4 mmHg*L-1*min, p < 0.01). This resulted in a more pronounced increase in MAP (mean change 1.7 ± 2.7 vs. 0.6 ± 2.8, p < 0.05), whereas the changes in SVI and CI were identical.

These data suggest that hypertensives are more susceptible to the vasoconstrictive effect of aldosterone. As this effect occurs as early as 15 minutes after the start of the aldosterone infusion it is a nongenomic effect, i.e. it is not mediated by the classical mineralocorticoid receptor. The importance of these effects in the pathogenesis of arterial hypertension remains to be established.