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Cardiovascular Research 1998 39(3):633-643; doi:10.1016/S0008-6363(98)00156-4
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Pulmonary and cardiac expression of preproendothelin-1 mRNA are increased in heart failure after myocardial infarction in rats. Localization of preproendothelin-1 mRNA and endothelin peptide

Theis Tønnessena,b,*, Per Kristian Lundea, Adel Giaidc, Ole M Sejersteda and Geir Christensena,d

aInstitute for Experimental Medical Research, University of Oslo, Ullevål Hospital, Oslo, Norway
bDepartment of Surgery, University of Oslo, Ullevål Hospital, Oslo, Norway
cDepartment of Pathology, McGill University, The Montreal General Hospital, Montreal, Canada
dDepartment of Medicine and Center for Molecular Genetics, University of California, San Diego, USA

* Corresponding author. Tel.: +47 22117800; Fax: +47 22117799; E-mail: theis.tonnessen@ioks.uio.no

Objectives: Recent reports indicate that endothelin (ET) plays an important pathophysiological role in congestive heart failure (CHF). However, existing data on local cardiopulmonary ET production are few. No studies have hitherto examined the specific anatomic localization of cardiopulmonary ET synthesis in CHF. Thus, the aims of the present study were to examine whether cardiopulmonary preproET-1 mRNA synthesis is upregulated in CHF and to determine the anatomic localization of preproET-1 mRNA and the mature peptide. Methods: CHF was induced in rats by occluding the left coronary artery. Only animals with a left ventricular end-diastolic pressure above 15 mmHg after one week were included (n=28). Sham-operated animals served as controls (n=24). Hearts and lungs were examined by mRNA slot blot analyses, in situ hybridization (ISH) and immunohistochemistry (IHC). Results: In CHF-rats, slot blot analyses revealed a 3.5±1.1-fold and a 6.4±0.8-fold upregulation of preproET-1 mRNA in the noninfarcted and the infarcted area of the left ventricles, respectively (p<0.05 for both). ISH revealed that the preproET-1 mRNA was localized predominantly over the granulation tissue in the infarcted region. The ET peptide was predominantly localized to inflammatory cells and remaining cardiomyocytes in the infarcted region as determined by IHC. Lungs from CHF-rats showed a 1.5±0.1-fold upregulation of preproET-1 mRNA (p=0.01). The most abundant preproET-1 mRNA and ET-1-like-immunoreactivity (ET-1-ir) was seen over inflammatory cells and over airway epithelial cells. Some ET-1-ir was also located to bronchial and vascular smooth muscle cells. Conclusion: Increased cardiopulmonary ET synthesis strongly suggest a pathophysiological role for ET in CHF.

KEYWORDS Endothelin; Heart failure; Ischemia; Rat


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