Negative inotropic effects of furosemide in the isolated rabbit heart: A prostaglandin-mediated event

Arthur M. Feldman, Michael A. Levine, Gary Gerstenblith, Keith D. Kaufman, Kenneth L. Baughman

Research output: Contribution to journalArticle


Furosemide is an effective diuretic that initiates a rapid diuresis and peripheral vasodilatation through renal adenylate cyclase inhibition and prostaglandin synthesis. Recently, it has been shown to be associated with activation of the neurohumoral vasoconstrictor mechanism and a further compromise of left ventricular function in patients with heart failure. The present study was performed to investigate the direct effects of furosemide on myocardial performance in the isolated perfused rabbit heart. Furosemide (10-3 M) caused a significant decrease in developed pressure as well as a similar fall in coronary perfusion pressure. Furosemide also decreased myocardial contractility when the coronary perfusion pressure was kept constant. The change in developed pressure but not the decrease in coronary perfusion pressure could be blocked by treatment with indomethacin. Furosemide did not antagonize rabbit cardiac membrane adenylate cyclase. Therefore, furosemide has a direct inhibitory effect on cardiac contractility that is related to prostaglandin synthesis.

Original languageEnglish (US)
Pages (from-to)493-499
Number of pages7
JournalJournal of cardiovascular pharmacology
Issue number4
StatePublished - Apr 1987


  • Adenylate cyclase
  • Cardiac function
  • Furosemide
  • Prostaglandins

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

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