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

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Aldosterone potentiates angiotensin II-induced signaling in vascular smooth muscle cells

Aldosteron potenziert die Angiotensin II-vermittelte Signaltransduktion in glatten Muskelzellen

Meeting Abstract (Hypertonie 2003)

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  • presenting/speaker I. Mazak
  • A. Fiebeler
  • D.N. Müller
  • J.K. Park
  • E. Shagdarsuren
  • C. Lindschau
  • R. Dechend
  • B. Pilz
  • H. Haller
  • F.C. Luft

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochV53

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/hoch2003/03hoch053.shtml

Published: November 11, 2004

© 2004 Mazak et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

Text

Background

In a double-transgenic human renin and human angiotensinogen rat model, we found that mineralocorticoid receptor (MR) blockade ameliorated angiotensin II (Ang II)-induced renal and cardiac damage with only a small effect on blood pressure. How Ang II and aldosterone (Ald) might interact is ill defined.

Methods and Results

We investigated the effects of Ang II (10-7 M) and Ald (10-7 M) on extracellular regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling in vascular smooth muscle cells (VSMC) with western blotting and confocal microscopy. Ang II induced ERK 1/2 and JNK phosphorylation by 2 min. Ald achieved the same by 10 min. Ang II+Ald had a potentiating effect by 2 min. The oxygen radical scavengers gluthatione (GSH) and Tiron as well as the specific epidermal growth factor (EGF) receptor antagonist AG1478, markedly reduced the Ang II-, Ald-, and combination-induced ERK1/2 phosphorylation. Preincubating the cells with the MR blocker spironolactone (Spi; 10-6 M) abolished Ang II-induced ERK1/2 phosphorylation.

Conclusion

Ald potentiates Ang II-induced ERK-1/2 and JNK phosphorylation. Oxygen radicals, the MR, and the EGF receptor play a role in early signaling induced by Ang II and Ald in VSMC. These in vitro data may help explain the effects of MR blockade on Ang II-induced end-organ damage in vivo.