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Angiotensin II contributes to isoproterenol-induced cardiomyocyte hypertrophy in normotensive mice

C. M. Santos M. W Chapleau; Lisete Compagno Michelini; Reunião Anual da Federação de Sociedades de Biologia Experimental, FeSBE (20. 2005 Águas de Lindóia, SP)

Resumos Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental, 2005

Águas de Lindóia, São Paulo Federação de Sociedades de Biologia Experimental 2005

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  • Título:
    Angiotensin II contributes to isoproterenol-induced cardiomyocyte hypertrophy in normotensive mice
  • Autor: C. M. Santos
  • M. W Chapleau; Lisete Compagno Michelini; Reunião Anual da Federação de Sociedades de Biologia Experimental, FeSBE (20. 2005 Águas de Lindóia, SP)
  • Assuntos: FISIOLOGIA
  • É parte de: Resumos Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental, 2005
  • Notas Locais: Disponível somente em CD-ROM
  • Descrição: Objetivo: The objective of this study was to test the hypothesis that angiotensin II (Ang II) contributes to left ventricular ( LV ) hypertrophy in mice chronically administered isoproterenol (ISO). Métodos e Resultados: Male C57BL/6J mice (20-25g) received tap water (VEH) with or without the AT1 receptor blocker losartan (LOS, ~30 mg/kg/day) to drink. Three days later, the mice were injected with ISO (12 mg/kg/day, sc. for 7 days) or VEH (50 µl olive oil). On the 5th day of ISO treatment, mice were instrumented for direct measurement of arterial pressure (AP). After recording AP in the conscious state, the mice were euthanized with sodium pentobarbital (80 mg/kg, ip). Hearts were removed, weighed, and prepared for histological analysis. The width of cardiomyocytes was measured from 20 randomly selected fields from 6-8 transmural slices/heart using a computer-based morphometric system. LOS and ISO treatments did not significantly change AP. ISO increased cardiomyocyte size by 27% in VEH-treated mice (n=7, P<.05), but failed to change myocyte size in LOS-treated mice (+8%, n=6, NS). In contrast, ISO increased LV mass to a similar extent in LOS-treated (+23%, P<.05) and VEH-treated (+29%, P<.05) mice. Conclusões: We conclude that blockade of AT1 receptors with LOS prevents ISO-induced cardiomyocyte hypertrophy in normotensive mice, implicating Ang II as a mediator of hypertrophy in this model. The dissociation between myocyte and LV hypertrophy
    with LOS treatment suggests additional changes in the composition of the heart in this model
  • Editor: Águas de Lindóia, São Paulo Federação de Sociedades de Biologia Experimental
  • Data de criação/publicação: 2005
  • Formato: res. 16.103.
  • Idioma: Português
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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