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| Item Type: | Article |
|---|---|
| Title: | Aldosterone potentiates angiotensin II-induced signaling in vascular smooth muscle cells |
| Creators Name: | Mazak, I., Fiebeler, A., Muller, D.N., Park, J.K., Shagdarsuren, E., Lindschau, C., Dechend, R., Viedt, C., Pilz, B., Haller, H. and Luft, F.C. |
| Abstract: | 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. How Ang II and aldosterone (Ald) might interact is ill defined. Methods and Results - We investigated the effects of Ang II (10-7 mol/L) and Ald (10 -7 mol/L) on extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling in vascular smooth muscle cells (VSMCs) with Western blotting and confocal microscopy. Ang II induced ERK 1/2 and JNK phosphorylation by 2 minutes. Ald achieved the same at 10 minutes. Ang II + Ald had a potentiating effect by 2 minutes. Two oxygen radical scavengers and the epidermal growth factor receptor (EGFR) antagonist AG1478 reduced Ang II-, Ald-, and combination-induced ERK1/2 phosphorylation. Preincubating the cells with the MR blocker spironolactone (10-6 mol/L) abolished Ang II-induced ROS generation, EGFR transactivation, and ERK1/2 phosphorylation. Conclusions - Ald potentiates Ang II-induced ERK-1/2 and JNK phosphorylation. Oxygen radicals, the MR, and the EGFR play a role in early signaling induced by Ang II and Ald in VSMCs. These in vitro data may help explain the effects of MR blockade on Ang II-induced end-organ damage in vivo. |
| Keywords: | Angiotensin, Aldosterone, Reactive Oxygen Species, Receptors, Kinases, Animals, Rats |
| Source: | Circulation |
| ISSN: | 0009-7322 |
| Publisher: | American Heart Association |
| Volume: | 109 |
| Number: | 22 |
| Page Range: | 2792-2800 |
| Date: | 8 June 2004 |
| Official Publication: | https://doi.org/10.1161/01.CIR.0000131860.80444.AB |
| PubMed: | View item in PubMed |
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