Endothelin (ET) is a endothelium-derived peptide with potent vasoconstrictor and growth-promoting actions. Although its physiological role remains unclear, recent studies report increased ET in various pathophysiological states, including congestive heart failure (CHF). The mechanisms contributing to increased ET in CHF probably include hemodynamic factors like increased atrial and venous pressures and reduced perfusion pressure and shear stress. Recent investigations also suggest that the kidney, lung, heart, and peripheral vasculature are sites of ET messenger RNA expression that may contribute to the elevation of ET in pathophysiological states. Recent studies have demonstrated that ET infusion to mimic pathophysiological levels has important biological actions, suggesting that ET may play an important role as a circulating hormone to maintain adequate perfusion during CHF. However, recent reports demonstrate that endogenous vasodilators like atrial natriuretic factor and endothelium-derived relaxing factor may attenuate ET actions in vivo. In conclusion, ET is a potent vasoconstricting and mitogenic peptide of endothelial origin that may participate in the adaptations to acute reductions in perfusion pressure in CHF. As this syndrome progresses, ET may contribute to the systemic vasoconstriction and cardiac vascular remodeling that characterize severe CHF. It is likely that therapeutic regimens that block or prevent the activation of ET or antagonize its actions may have a beneficial role in the treatment of heart failure.
|Original language||English (US)|
|Issue number||5 SUPPL. V|
|State||Published - 1993|
- blood pressure
- heart failure, congestive
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine