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Endothelin and Ca++ agonist Bay K 8644: different vasoconstrictive properties
M Auguet1, S Delaflotte, P E Chabrier
1Institut Henri Beaufour, Les Ulis, France.
Biochemical and Biophysical Research Communications
|October 14, 1988
Summary
Endothelin causes vasoconstriction in rat aorta differently than Bay K 8644. Endothelin likely acts via specific receptors, not by activating calcium channels.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
Background:
- Endothelin is a potent vasoconstrictor peptide.
- The precise mechanism of endothelin-induced vasoconstriction, particularly its interaction with calcium channels, requires further elucidation.
Purpose of the Study:
- To investigate the mechanism of endothelin-induced vasoconstriction in rat isolated aorta.
- To compare endothelin's mechanism with that of the calcium channel agonist Bay K 8644.
Main Methods:
- Isolated rat aorta preparations were used.
- Vascular contractions were measured in response to endothelin and Bay K 8644.
- Experiments were conducted in normal, K+-depolarized, and calcium-free media.
- The effects of calcium antagonists (nifedipine, diltiazem, D600) and intracellular calcium depletion (phenylephrine) were assessed.
Main Results:
- Endothelin induced a slow, sustained contraction (EC50 = 4 nM) in normal medium.
- Bay K 8644 induced a fast, rhythmic contraction (EC50 = 14 nM) in K+-depolarized medium.
- Endothelin-induced contractions were not inhibited by nifedipine, diltiazem, or D600.
- Endothelin's effect persisted in calcium-free medium and after intracellular calcium depletion.
Conclusions:
- Endothelin does not activate voltage-dependent calcium channels.
- Endothelin-mediated vasoconstriction likely involves specific endothelin receptors.
- These findings differentiate endothelin's mechanism from that of L-type calcium channel agonists.