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Functional evidence for different endothelin receptors in the lung
H L Lippton1, T A Hauth, G A Cohen
1Department of Internal Medicine, Louisiana State University Medical School, New Orleans.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|July 1, 1993
Summary
Endothelin (ET)-1 and ET-2 cause tachyphylaxis in pulmonary and systemic vasodilation, unlike ET-3. ET-3
Area of Science:
- Cardiovascular Physiology
- Pulmonary Circulation
- Vascular Pharmacology
Background:
- Endothelin (ET) isoforms are potent vasoactive peptides.
- Understanding their distinct vascular effects and receptor interactions is crucial.
Purpose of the Study:
- To compare pulmonary and systemic vascular responses to ET-1, ET-2, and ET-3.
- To investigate tachyphylaxis and cross-tachyphylaxis of ET isoforms.
Main Methods:
- Intact spontaneously breathing cat model.
- Constant pulmonary blood flow and left atrial pressure.
- Intralobar infusions and bolus injections of ET isoforms and U-46619.
Main Results:
- ET-1 and ET-2 initially caused vasodilation, but repeated doses led to vasoconstriction (tachyphylaxis).
- ET-3 induced pulmonary vasodilation resistant to tachyphylaxis, while systemic vasodilation was lost.
- Cross-tachyphylaxis observed for ET-1 and ET-2, but not for ET-3.
Conclusions:
- Pulmonary and systemic vasodilator responses to ET-1 and ET-2 exhibit tachyphylaxis and cross-tachyphylaxis.
- Pulmonary ET-3 vasodilation is resistant to tachyphylaxis, suggesting distinct receptor mechanisms.
- Data support the existence of at least two ET receptor subtypes (ETA-like and ETC-like) in the pulmonary vasculature.