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Ca(2+)-activated Cl(-) current can be triggered by Na(+) current-induced SR Ca(2+) release in rabbit ventricle.

H Sun¹, D Chartier, S Nattel

¹Research Centre, Montréal Heart Institute, Montreal H1T 1C8.

The American Journal of Physiology

|October 12, 1999

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The study shows that sodium current (I(Na)) can activate calcium-activated chloride current (I(Cl(Ca))) in rabbit heart cells, even without the typical L-type calcium current (I(Ca(L))). This suggests a new pathway for regulating heart cell electrical activity.

Area of Science:

Cardiology
Electrophysiology
Molecular Physiology

Background:

The calcium-activated chloride current (I(Cl(Ca))) is crucial for cardiac action potential repolarization.
Typically, I(Cl(Ca)) is activated by calcium release from the sarcoplasmic reticulum (SR), primarily triggered by L-type calcium current (I(Ca(L))).
Emerging evidence suggests sodium current (I(Na)) might also influence SR calcium release via reverse-mode Na+/Ca2+ exchange.

Purpose of the Study:

To investigate if I(Cl(Ca)) can be induced by I(Na) independently of I(Ca(L)).

Main Methods:

Whole-cell patch-clamp technique and Indo-1 fluorescence measurements in rabbit ventricular myocytes.
Pharmacological blockade of I(Ca(L)) using nicardipine.
Recording of macroscopic currents and intracellular calcium transients under varying ionic conditions.

Related Experiment Videos

Main Results:

A 4-aminopyridine-resistant outward current, consistent with I(Cl(Ca)), was observed in 64/81 myocytes when I(Ca(L)) was blocked.
This current accompanied a phasic intracellular calcium transient and exhibited reversal potentials matching predicted chloride (Cl(-)) gradients.
The current and calcium transient were sensitive to niflumic acid, caffeine, ryanodine, tetrodotoxin, and extracellular calcium removal, confirming their I(Cl(Ca)) and SR-dependent nature.

Conclusions:

I(Cl(Ca)) can be effectively recorded in cardiac myocytes even when I(Ca(L)) is absent.
An I(Na)-induced SR calcium release mechanism exists in the rabbit heart.
This pathway may play a significant physiological role in activating the calcium-sensitive membrane chloride conductance.