Abstract
Excess aldosterone promotes pathological remodeling of the heart and imbalance in cardiac ion homeostasis of sodium, potassium and calcium. Novel treatment with proanthocyanidins in aldosterone-treated rats has resulted in downregulation of cardiac SGK1, the main genomic aldosterone-induced intracellular mediator of ion handling. It therefore follows that proanthocyanidins could be modulating cardiac ion homeostasis in aldosterone-treated rats. Male Wistar rats received aldosterone (1 mg kg−1 day−1) +1% NaCl for three weeks. Half of the animals in each group were simultaneously treated with the proanthocyanidins-rich extract (80% w/w) (PRO80, 5 mg kg−1 day−1). PRO80 prevented cardiac hypertrophy and decreased calcium content. Expression of ion channels (ROMK, NHE1, NKA and NCX1) and calcium transient mediators (CAV1.2, pCaMKII and oxCaMKII) were reduced by PRO80 treatment in aldosterone-treated rats. To conclude, our data indicate that PRO80 may offer an alternative treatment to conventional MR-blockade in the prevention of aldosterone-induced cardiac pathology.
Highlights
The development of cardiac hypertrophy is frequently accompanied by an imbalance in sodium, potassium and calcium homeostasis leading to alterations in ion currents thereby contributing to development of ventricular dysfunction and arrhythmias [6,7]
Excess aldosterone promotes pathological remodeling of the heart and an imbalance in cardiac ion homeostasis leading to the development of cardiac hypertrophy, heart failure and arrhythmias [10,11,12,13]
We show that PRO80 blocked the aldosterone-induced changes in cardiac ROMK, NCX1, Na+ /K+ ATPase pump (NKA) (α1 subunit), NHE1, Cav1.2 (α1C subunit), pCAMKII, oxCamKII and protein expression and cardiac calcium content
Summary
Chronic and severe hypertension leads to cardiac hypertrophy and, eventually, heart failure [3,4,5]. The development of cardiac hypertrophy is frequently accompanied by an imbalance in sodium, potassium and calcium homeostasis leading to alterations in ion currents thereby contributing to development of ventricular dysfunction and arrhythmias [6,7]. Such imbalance in electrolyte homeostasis is, at least in part, a consequence of changes in the expression and activity of key proteins involved in cardiomyocyte ion transport [8,9]. Excess aldosterone promotes pathological remodeling of the heart and an imbalance in cardiac ion homeostasis leading to the development of cardiac hypertrophy, heart failure and arrhythmias [10,11,12,13]
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