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Provedor de dados:  BJMBR
País:  Brazil
Título:  Chronic hypertension alters the expression of Cx43 in cardiovascular muscle cells
Autores:  Haefliger,J.-A.
Meda,P.
Data:  2000-04-01
Ano:  2000
Palavras-chave:  Cell-cell communication
Gap junctions
Connexins
Vasculature
Heart
Hypertension
Blood pressure
Renin
Deoxycorticosterone
Nitric oxide
Distensibility
Resumo:  Connexin43 (Cx43), the predominant gap junction protein of muscle cells in vessels and heart, is involved in the control of cell-to-cell communication and is thought to modulate the contractility of the vascular wall and the electrical coupling of cardiac myocytes. We have investigated the effects of arterial hypertension on the expression of Cx43 in aorta and heart in three different models of experimental hypertension. Rats were made hypertensive either by clipping one renal artery (two kidney, one-clip renal (2K,1C) model) by administration of deoxycorticosterone and salt (DOCA-salt model) or by inhibiting nitric oxide synthase with NG-nitro-L-arginine methyl ester (L-NAME model). After 4 weeks, rats of the three models showed a similar increase in intra-arterial mean blood pressure and in the thickness of the walls of both aorta and heart. Analysis of heart mRNA demonstrated no change in Cx43 expression in the three models compared to their respective controls. The same 2K,1C and DOCA-salt hypertensive animals expressed twice more Cx43 in aorta, and the 2K,1C rats showed an increase in arterial distensibility. In contrast, the aortae of L-NAME hypertensive rats were characterized by a 50% decrease in Cx43 and the carotid arteries did not show increased distensibility. Western blot analysis indicated that Cx43 was more phosphorylated in the aortae of 2K,1C rats than in those of L-NAME or control rats, indicating a differential regulation of aortic Cx43 in different models of hypertension. The data suggest that localized mechanical forces induced by hypertension affect Cx43 expression and that the cell-to-cell communication mediated by Cx43 channels may contribute to regulating the elasticity of the vascular wall.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2000000400009
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X2000000400009
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.33 n.4 2000
Direitos:  info:eu-repo/semantics/openAccess
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