Abstract 1: Deletion of the Mapk-p38 From Vascular Smooth Muscle Cells and Cardiomyocytes Causes Hypotension and Dilated Cardiomyopathy in Angiotensin II Dependent Hypertension

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2013-09, Vol.62 (suppl_1)
• Main Authors: Mende, Susanne, Bottermann, Katharina, Stamer, Stefanie, Thieme, Manuel, Gödecke, Axel, Park, Joon-Keun, Rump, Lars Christian, Stegbauer, Johannes
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.62.suppl_1.A1

Abstract only The heart and the vasculature are key targets of angiotensin (Ang) II. In this regard, Ang II acting via Ang II type 1 (AT1)-receptors induces hypertension, cardiac hypertrophy and vascular injury. Since AT1-receptor stimulation have been shown to activate the mitogen activated protein kinase (MAPK) p38 leading to hypertrophy, migration and remodelling in cardiomocytes and vascular smooth muscle cells (VSMC)s in vitro, the MAPK p38 is considered as a major contributor in Ang II mediated cardiac and vascular injury. In order to investigate its role in Ang II dependent hypertension, we generated mice lacking p38alpha only in VSMC and cardiomyocytes (p38KO) using Cre-Loxp technology with a KISM22-cre transgene on a Bl6/C57 background. The specificity of p38alpha deletion was verified by western blot analysis. While cardiac function did not differ between both groups, blood pressures (BPs) were significantly lower under baseline conditions in p38KO mice compared to controls (106.4±5.2 vs. 123.6±5.4 mmHg; p