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Cardiovascular Research Advance Access first published online on March 20, 2009
This version [Corrected Proof] published online on April 9, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp099
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

KATP activation prevents progression of cardiac hypertrophy to failure induced by pressure overload via protecting endothelial function

Shan Gao1,2,{dagger}, Chao-Liang Long1,{dagger}, Ru-Huan Wang3 and Hai Wang1,3,4,*

1 Department of Cardiovascular Pharmacology, Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China
2 Department of Pharmacology, Anhui Medical University, Hefei 230032, Anhui, China
3 Thadweik Academy of Medicine, Beijing 100039, China
4 Department of Environmental Medicine, Tianjin Institute of Hygiene and Environmental Medicine, Tianjin 300050, China

* Corresponding author. Tel: +86 10 6693 2651; fax: +86 10 6816 8180; E-mail address: wh9588{at}yahoo.com.cn

Aims: We investigated the effects of iptakalim, a new ATP-sensitive potassium channel (KATP) opener providing endothelial protection, on the progression of cardiac hypertrophy to failure in a rat model of pressure overloading caused by abdominal aortic banding (AAB). Endothelial dysfunction is central to cardiac hypertrophy and failure induced by pressure overload. It would be useful to clarify whether iptakalim could prevent this.

Methods and results: The effects of pressure overload were assessed in male Sprague–Dawley rats 6 weeks after AAB using progression of cardiac hypertrophy to heart failure as the endpoint. The AAB-treated rats had significantly elevated blood pressure, systolic and diastolic cardiac dysfunction, evidence of left ventricular hypertrophy (LVH), and transition to heart failure. LVH was characterized by increases in the ratios of heart and left ventricular weights to body weight, increased myocyte cross-sectional areas, myocardial and perivascular fibrosis, and elevated cardiac hydroxyproline. These could be prevented by treatment with iptakalim at daily oral doses of 1, 3, and 9 mg/kg for 6 weeks. Progression to cardiac failure, demonstrated by increases in relative lung and right ventricular weights, cardiac function disorders and overexpression of atrial and B-type natriuretic peptide mRNA, could also be prevented. The downregulated nitric oxide signalling system was enhanced, whereas the upregulated endothelin signalling system was inhibited, resulting in normalization of the balance between these two systems.

Conclusion: Iptakalim protected the endothelium and prevented progression of cardiac hypertrophy to failure induced by a pressure overload.

KEYWORDS Pressure overload; ATP-sensitive potassium channel opener; Iptakalim; Cardiac remodelling; Endothelial function

Time for primary review: 20 days

{dagger} Drs S.G. and C.-L.L. contributed equally to this work.


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