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Impact of AT2 Receptor Deficiency on Postnatal Cardiovascular Development

Please always quote using this URN: urn:nbn:de:bvb:20-opus-134902
  • Background: The angiotensin II receptor subtype 2 (AT2 receptor) is ubiquitously and highly expressed in early postnatal life. However, its role in postnatal cardiac development remained unclear. Methodology/Principal Findings: Hearts from 1, 7, 14 and 56 days old wild-type (WT) and AT2 receptor-deficient (KO) mice were extracted for histomorphometrical analysis as well as analysis of cardiac signaling and gene expression. Furthermore, heart and body weights of examined animals were recorded and echocardiographic analysis of cardiac functionBackground: The angiotensin II receptor subtype 2 (AT2 receptor) is ubiquitously and highly expressed in early postnatal life. However, its role in postnatal cardiac development remained unclear. Methodology/Principal Findings: Hearts from 1, 7, 14 and 56 days old wild-type (WT) and AT2 receptor-deficient (KO) mice were extracted for histomorphometrical analysis as well as analysis of cardiac signaling and gene expression. Furthermore, heart and body weights of examined animals were recorded and echocardiographic analysis of cardiac function as well as telemetric blood pressure measurements were performed. Moreover, gene expression, sarcomere shortening and calcium transients were examined in ventricular cardiomyocytes isolated from both genotypes. KO mice exhibited an accelerated body weight gain and a reduced heart to body weight ratio as compared to WT mice in the postnatal period. However, in adult KO mice the heart to body weight ratio was significantly increased most likely due to elevated systemic blood pressure. At postnatal day 7 ventricular capillarization index and the density of \(\alpha\)-smooth muscle cell actin-positive blood vessels were higher in KO mice as compared to WT mice but normalized during adolescence. Echocardiographic assessment of cardiac systolic function at postnatal day 7 revealed decreased contractility of KO hearts in response to beta-adrenergic stimulation. Moreover, cardiomyocytes from KO mice showed a decreased sarcomere shortening and an increased peak Ca\(^{2+}\) transient in response to isoprenaline when stimulated concomitantly with angiotensin II. Conclusion: The AT2 receptor affects postnatal cardiac growth possibly via reducing body weight gain and systemic blood pressure. Moreover, it moderately attenuates postnatal vascularization of the heart and modulates the beta adrenergic response of the neonatal heart. These AT2 receptor-mediated effects may be implicated in the physiological maturation process of the heart.show moreshow less

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Metadaten
Author: Daniel Biermann, Andreas Heilmann, Michael Didié, Saskia Schlossarek, Azadeh Wahab, Michael Grimm, Maria Römer, Hermann Reichenspurner, Karim R. Sultan, Anna Steenpass, Süleyman Ergün, Sonia Donzelli, Lucie Carrier, Heimo Ehmke, Wolfram H. Zimmermann, Lutz Hein, Rainer H. Böger, Ralf A. Benndorf
URN:urn:nbn:de:bvb:20-opus-134902
Document Type:Journal article
Faculties:Medizinische Fakultät / Institut für Anatomie und Zellbiologie
Language:English
Parent Title (English):PLoS One
Year of Completion:2012
Volume:7
Issue:10
Pagenumber:e47916
Source:PLoS ONE 7(10): e47916. doi:10.1371/journal.pone.0047916
DOI:https://doi.org/10.1371/journal.pone.0047916
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Tag:II type-2 receptor; angiotensin II; blood pressure; cardiac hyperthrophy; chronic kidney disease; human endothelial cells; in vitro; mice; rat heart; tube formation
Release Date:2017/12/17
Licence (German):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung