Aldosterone augments endothelin-1-induced cardiac myocyte hypertrophy with the reinforcement of the JNK pathway.
Aldosterone is thought to regulate cardiac work independently of sodium retention, though the mechanisms remain to be known. In the present study, we have demonstrated that aldosterone reinforces endothelin-mediated cardiac hypertrophy with the increase in cell surface area and upregulation of the transcripts characteristic of hypertrophy. We have also shown that aldosterone augments c-Jun N-terminal kinase activation induced by endothelin-1. Taken together, it is suggested that aldosterone modulates cardiac hypertrophy, at least partially, synergistically with extracellular signals that have been shown to be involved in cardiac remodeling.
Department of Molecular Medicine, Osaka University Graduate School of Medicine, Suita City, Osaka, Japan.
Yuichi
Y
Oshima
Yasushi
Y
Fujio
Masanobu
M
Funamoto
Shinji
S
Negoro
Masahiro
M
Izumi
Yoshikazu
Y
Nakaoka
Hisao
H
Hirota
Keiko
K
Yamauchi-Takihara
Ichiro
I
Kawase
D000450:Aldosterone / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D006332:Cardiomegaly / Q000503:physiopathology*; D002478:Cells, Cultured; D019332:Endothelin-1 / Q000502:physiology*; D004789:Enzyme Activation; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D010766:Phosphorylation; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism
D019332:Endothelin-1; D000450:Aldosterone; D012964:Sodium; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases