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1 Johannes-Mueller-Institut fuer Physiologie, Humboldt-Universitaet, Berlin, Berlin, Germany
2 Innere Medizin, Kardiologie, Campus Virchow Klinikum, Humboldt-Universitaet, Berlin, Berlin, Germany
3 Klinik fuer Herz-, Thorax- und Gefaesschirurgie, Deutsches Herzzentrum Berlin, Berlin, Berlin, Germany
4 Exercise Science, The University of Iowa, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: harald-stauss{at}uiowa.edu.
Enhanced blood pressure variability contributes to left ventricular hypertrophy and end organ damage even in the absence of hypertension. We hypothesized that the greater number of high blood pressure episodes associated with enhanced blood pressure vari-ability causes cardiac hypertrophy and dysfunction by activation of mechanosensitive and autocrine pathways. Normotensive mice were subjected to sinoaortic baroreceptor denervation (SAD) or sham surgery. Twelve weeks later, blood pressure variability was doubled in SAD com-pared to sham-operated mice. Blood pressure did not differ. Cardiac hypertrophy was reflected in greater heart to body weight ratios, larger myocyte cross-sectional areas, and more left ventricular collagen deposition. Furthermore, left ventricular atrial and brain natriuretic peptide mRNA expression was greater in SAD than in sham-operated mice. SAD had higher left ventricular end-diastolic pressures and lower myocardial con-tractility indices, indicating cardiac dysfunction. Cardiac protein content of phosphory-lated p125 focal adhesion kinase (p125 FAK) and phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) were greater in SAD than in sham-operated mice, indicating activation of mechanosensitive pathways of cardiac hypertrophy. Further-more, enhanced cardiac renin and transforming growth factor-beta1 (TGFbeta1) protein content indicates activation of autocrine pathways of cardiac hypertrophy. Adrenal tyro-sine hydroxylase protein content and the number of renin positive glomeruli were not different, suggesting that sympathetic activation and the systemic renin-angiotensin sys-tem did not contribute to cardiac hypertrophy. In conclusion, more frequent blood pressure rises in subjects with high blood pressure variability activate mechanosensitive and autocrine pathways leading to cardiac hyper-trophy and dysfunction even in the absence of hypertension.
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