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Cardiovascular Research 2002 53(4):963-970; doi:10.1016/S0008-6363(01)00558-2
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Chronic endothelin receptor blockade prevents renal vasoconstriction and sodium retention in rats with chronic heart failure

Shuang-Shuang Dinga,b, Changbin Qiua,b, Patrick Hessa, Jian-Fei Xia,b, Jean-Paul Clozela and Martine Clozela,*

aActelion Pharmaceuticals Ltd., CH-4123 Allschwil, Switzerland
bDepartment of Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 200031, China

martine.clozel{at}actelion.com

* Corresponding author. Tel.: +41-61-487-4513; fax: +41-61-487-4500

Objective: Importance of endothelin in mediating the chronic renal alterations of chronic heart failure was studied in rats chronically treated with bosentan after myocardial infarction. Methods: Rats were subjected to coronary artery ligation and were treated for 8 weeks with placebo or bosentan, a dual ETA and ETB receptor antagonist, (~100 mg/kg/day) as food admix. Sham-operated rats served as normal controls. Cardiac and renal functions were measured at the end of 8-week treatment. Results: Bosentan significantly reduced the elevated left ventricular end-diastolic pressure (from 26.6±3.3 to 11.4±2.2 mmHg, P<0.001) and the increased heart-to-body-weight ratio seen in untreated rats with myocardial infarction. Bosentan prevented the marked increase in renal vascular resistance (bosentan, 7.7±0.6; untreated, 15.6±2.5 mmHg/ml/min; P<0.001). This led to a significant increase in renal plasma flow resulting in a decrease in filtration fraction. Bosentan furthermore increased urinary sodium excretion. Conclusions: Prolonged ET receptor blockade in rats with myocardial infarction has chronic renal vasodilatory effect and improves renal sodium excretory function. Thus, dual ET antagonists such as bosentan might be useful in the treatment of the progressive renal failure associated with human chronic heart failure.

KEYWORDS Endothelins; Heart failure; Infarction; Renal function; Vasoactive agents


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