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Endothelin-1 inhibits pacemaker currents in rabbit SA node cells

H Tanaka¹, Y Habuchi, M Nishio

¹Department of Laboratory Medicine, Kyoto Prefectural University of Medicine, Japan.

Journal of Cardiovascular Pharmacology

|May 22, 1998

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Endothelin-1 (ET-1) inhibits heart pacemaker activity by reducing T-type calcium (ICa,T) and hyperpolarization-activated inward currents (I(f)) in rabbit sinoatrial node cells. These findings reveal new mechanisms for ET-1's negative chronotropic effects.

Area of Science:

Cardiovascular Physiology
Electrophysiology
Pharmacology

Background:

Endothelin-1 (ET-1) is known to affect cardiac function.
Previous studies indicated ET-1 influences sinoatrial (SA) node cells.
The precise ionic mechanisms of ET-1's chronotropic effects require further elucidation.

Purpose of the Study:

To investigate the effects of ET-1 on specific ion currents in SA node pacemaker cells.
To identify additional ionic mechanisms contributing to ET-1-induced negative chronotropy.

Main Methods:

Whole-cell patch-clamp technique applied to rabbit SA node cells.
Concentration-response analysis of ET-1 effects on ICa,T and I(f).
Assessment of ET-1's action in the presence of the ET-1 receptor antagonist BQ485.

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Main Results:

ET-1 significantly reduced the T-type calcium current (ICa,T) and the hyperpolarization-activated inward current (I(f)).
These inhibitory effects were concentration-dependent, with low EC50 values (0.9 nM for ICa,T; 2.3 nM for I(f)).
ET-1's effects on ICa,T and I(f) were blocked by BQ485, confirming receptor-mediated action.

Conclusions:

ET-1 exerts negative chronotropic effects on rabbit SA node cells through additional mechanisms beyond previously identified currents.
Inhibition of ICa,T and I(f) represents novel pathways for ET-1's modulation of cardiac pacemaker activity.
These findings deepen the understanding of ET-1's role in regulating heart rate.