Circulation journal : official journal of the Japanese Circulation Society · 2009
Effects of aldosterone on Cx43 gap junction expression in neonatal rat cultured cardiomyocytes.
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Suzuki Shinsuke, Ohkusa Tomoko, Sato Takashi, Yoshida Masaaki, Yasui Kenji, Miwa Keiko, Lee Jong-Kook, Yano Masafumi, Kodama Itsuo, Matsuzaki Masunori
Аннотация
BACKGROUND: The renin-angiotensin-aldosterone system affects cellular morphology and function in the heart under a variety of pathologic conditions. In the present study the effects of aldosterone on the expression of connexin (Cx) 43 gap junctions in cardiomyocytes were investigated.
METHODS AND RESULTS: Cultured rat ventricular myocytes were exposed to aldosterone for 24 h. The protein and mRNA expression of Cx43 was estimated. Propagation of excitation was visualized by a multiple electrode array system. Treatment of the myocytes with 10(-8) mol/L aldosterone resulted in a significant upregulation of Cx43 (by approximately 1.5-fold in protein and by approximately 1.2-fold in mRNA). The immunoreactive signal of Cx43 was also increased. Conduction velocity (CV) was increased by approximately 24%. Treatment of the myocytes with aldosterone at higher concentrations (10(-6)-10(-4) mol/L) caused a significant downregulation of Cx43 protein (by approximately 0.3-fold) without affecting Cx43 mRNA levels, and decreased the CV by ~23%. The Cx43 upregulation and CV acceleration at 10(-8) mol/L aldosterone were prevented by pretreatment with eplerenone, but unaffected by mifepristone. Pretreatment of the myocytes with eplerenone or mifepristone did not prevent the Cx43 downregulation by aldosterone at 10(-6)-10(-4) mol/L.
CONCLUSIONS: Aldosterone may be involved in arrhythmogenic gap junction remodeling through its dual effects on the expression of Cx43.
METHODS AND RESULTS: Cultured rat ventricular myocytes were exposed to aldosterone for 24 h. The protein and mRNA expression of Cx43 was estimated. Propagation of excitation was visualized by a multiple electrode array system. Treatment of the myocytes with 10(-8) mol/L aldosterone resulted in a significant upregulation of Cx43 (by approximately 1.5-fold in protein and by approximately 1.2-fold in mRNA). The immunoreactive signal of Cx43 was also increased. Conduction velocity (CV) was increased by approximately 24%. Treatment of the myocytes with aldosterone at higher concentrations (10(-6)-10(-4) mol/L) caused a significant downregulation of Cx43 protein (by approximately 0.3-fold) without affecting Cx43 mRNA levels, and decreased the CV by ~23%. The Cx43 upregulation and CV acceleration at 10(-8) mol/L aldosterone were prevented by pretreatment with eplerenone, but unaffected by mifepristone. Pretreatment of the myocytes with eplerenone or mifepristone did not prevent the Cx43 downregulation by aldosterone at 10(-6)-10(-4) mol/L.
CONCLUSIONS: Aldosterone may be involved in arrhythmogenic gap junction remodeling through its dual effects on the expression of Cx43.