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Endothelin-1 in heart and pulmonary tissue in experimental heart failure

M L Sirviö1, K Helin, P Stewen

  • 1Unit of Clinical Physiology, Minerva Foundation, Helsinki, Finland.

Blood Pressure
|July 1, 1997
PubMed

Insights

Congestive heart failure (CHF) increases levels of endothelin 1 (ET-1) in lung and right ventricle tissues. This enhanced ET-1 production may contribute to pulmonary vascular resistance in CHF patients.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Pathophysiology

Background:

  • Congestive heart failure (CHF) is a complex syndrome affecting cardiac function.
  • Endothelin 1 (ET-1) is a potent vasoconstrictor peptide implicated in cardiovascular diseases.
  • The role of ET-1 in the specific tissue alterations during CHF requires further elucidation.

Purpose of the Study:

  • To investigate the impact of experimentally induced CHF on tissue levels of ET-1 and its precursor mRNA (prepro-ET-1) in rats.
  • To determine the specific cardiac and pulmonary compartments affected by these changes.

Main Methods:

  • Congestive heart failure (CHF) was induced in rats via left coronary artery ligation.
  • Tissue levels of ET-1 were quantified using radioimmunoassay.
  • Prepro-ET-1 mRNA levels were assessed via quantitative polymerase chain reaction.
  • Cardiac and pulmonary tissues, along with plasma atrial natriuretic peptide, were analyzed three weeks post-ligation.

Main Results:

  • Rats with CHF exhibited increased heart weight/body weight ratio and elevated plasma atrial natriuretic peptide.
  • Pulmonary tissue showed a 3.6-fold increase in ET-1 concentration.
  • The right ventricle displayed a 1.4-fold increase in ET-1 concentration, while the left ventricle did not show significant changes.
  • Prepro-ET-1 mRNA levels mirrored the observed ET-1 concentration patterns.

Conclusions:

  • Experimentally induced CHF leads to enhanced ET-1 production in pulmonary and right ventricular tissues.
  • Elevated ET-1 in these tissues may play a significant role in the development of high pulmonary vascular resistance associated with CHF.
  • These findings highlight a potential therapeutic target for managing CHF complications.

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