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ET-1 stimulates Ca2+ currents in cardiac cells
1Department of Physiology and Biophysics, Faculty of Medicine, University of Sherbrooke, Québec, Canada.
Journal of Cardiovascular Pharmacology
|January 1, 1995
Summary
Endothelin-1 (ET-1) stimulates T- and L-type calcium currents in human and chick heart cells via ET(A) receptors and a G-protein. This effect on cardiac calcium channels was confirmed using electrophysiology.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Ion Channel Function
Background:
- Endothelin-1 (ET-1) is a potent vasoconstrictor peptide.
- Its role in regulating cardiac ion channel activity is not fully elucidated.
- Understanding ET-1's effects on cardiac cells is crucial for cardiovascular research.
Purpose of the Study:
- To investigate the effects of Endothelin-1 (ET-1) on ion currents in human and chick ventricular cells.
- To determine the specific receptor subtype and signaling pathway involved in ET-1's action.
Main Methods:
- Whole-cell voltage-clamp technique was employed to measure ion currents.
- Experiments were conducted on isolated human and chick ventricular single cells.
- Pharmacological agents, including ET(A) receptor antagonist BQ123 and pertussis toxin (PTX), were used.
Main Results:
- ET-1 dose-dependently stimulated both T-type and L-type calcium (Ca2+) currents.
- ET-1 had no significant effect on fast sodium (Na+) or delayed outward potassium (K+) currents.
- The stimulatory effect of ET-1 was blocked by BQ123 and prevented by PTX treatment.
Conclusions:
- Functional Endothelin ET(A) receptors are present in human and chick ventricular cells.
- ET-1 enhances cardiac T- and L-type Ca2+ currents.
- This stimulation is mediated by a pertussis toxin-sensitive G-protein signaling pathway.