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K(ATP) activation prevents progression of cardiac hypertrophy to failure induced by pressure overload via protecting endothelial function.
Cardiovasc Res. 2009 Aug 01; 83(3):444-56.CR

Abstract

AIMS

We investigated the effects of iptakalim, a new ATP-sensitive potassium channel (K(ATP)) 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.

Authors+Show Affiliations

Department of Cardiovascular Pharmacology, Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19304734

Citation

Gao, Shan, et al. "K(ATP) Activation Prevents Progression of Cardiac Hypertrophy to Failure Induced By Pressure Overload Via Protecting Endothelial Function." Cardiovascular Research, vol. 83, no. 3, 2009, pp. 444-56.
Gao S, Long CL, Wang RH, et al. K(ATP) activation prevents progression of cardiac hypertrophy to failure induced by pressure overload via protecting endothelial function. Cardiovasc Res. 2009;83(3):444-56.
Gao, S., Long, C. L., Wang, R. H., & Wang, H. (2009). K(ATP) activation prevents progression of cardiac hypertrophy to failure induced by pressure overload via protecting endothelial function. Cardiovascular Research, 83(3), 444-56. https://doi.org/10.1093/cvr/cvp099
Gao S, et al. K(ATP) Activation Prevents Progression of Cardiac Hypertrophy to Failure Induced By Pressure Overload Via Protecting Endothelial Function. Cardiovasc Res. 2009 Aug 1;83(3):444-56. PubMed PMID: 19304734.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - K(ATP) activation prevents progression of cardiac hypertrophy to failure induced by pressure overload via protecting endothelial function. AU - Gao,Shan, AU - Long,Chao-Liang, AU - Wang,Ru-Huan, AU - Wang,Hai, Y1 - 2009/03/20/ PY - 2009/3/24/entrez PY - 2009/3/24/pubmed PY - 2009/9/18/medline SP - 444 EP - 56 JF - Cardiovascular research JO - Cardiovasc Res VL - 83 IS - 3 N2 - AIMS: We investigated the effects of iptakalim, a new ATP-sensitive potassium channel (K(ATP)) 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. SN - 1755-3245 UR - https://www.unboundmedicine.com/medline/citation/19304734/K_ATP__activation_prevents_progression_of_cardiac_hypertrophy_to_failure_induced_by_pressure_overload_via_protecting_endothelial_function_ L2 - https://academic.oup.com/cardiovascres/article-lookup/doi/10.1093/cvr/cvp099 DB - PRIME DP - Unbound Medicine ER -