Aldosteron and end-organ damage

Aldosteron and end-organ damage
	Several clinical studies have shown that blocking the action of aldosterone with mineralocorticoid receptor (MR) blockers in addition to angiotensin (Ang) II inhibitors reduces the mortality of patients with ischemic heart disease by further 30 %. Recent animal data suggest that is a main pathogenic factor for the development of end-organ damage. The role of locally produced and its receptor MR is not well understood. We have shown in vitro can potentiate Ang II-induced early signaling. The conjoining pathway for this interaction has not been characterized so far and the role of the MR remains to be illucidated.
Head of Project:
	PD Dr. Dominik Müller Charité - Universitätsmedizin Berlin Department of Internal Medicine, Nephrology and Hypertensiology CBB
Additional Member of Project:
	Dr. Erdenechimeg Günther, Dr. Anette Fiebeler, PD Dr. Ralf Dechend
Begin/End of Project:
	07/2004 - 06/2008
Funded by:
	BMBF
Scienceclassification:
	n.a.
Online-Information:
	http://www.gesundheitsforschung-bmbf.de/de/908.php
Publications:
	Fiebeler A, Nussberger J, Shagdarsuren E, Rong S, Hilfenhaus G, Al-Saadi N, Dechend R, Wellner M, Meiners S, Maser-Gluth C, Jeng AY, Webb RL, Luft FC, Muller DN. An aldosterone synthase inhibitor ameliorates angiotensin II-induced organ damage. Circulation 2005;111:3087-94. Shagdarsuren E, Wellner M, Braesen J-H, Park J-K, Fiebeler A, Henke N, Dechend R, Gratze P, Luft FC, Müller, DN. Complement activation in angiotensin II-induced organ damage. Circ Res 2005;97:716-24. Mazak I, Fiebeler A, Muller DN, Park J-K, Shagdarsuren E, Lindschau C, Dechend R, Pilz B, Haller H, Luft FC. Aldosterone potentiates angiotensin II-induced signaling in vascular smooth muscle cells. Circulation 2004;109:2792-2800.