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Gating in iodate-modified single cardiac Na+ channels.
M Kohlhardt1, H Fichtner, U Fröbe
1Physiological Institute, University Freiburg, West Germany.
The Journal of Membrane Biology
|November 1, 1989
Summary
Chemicals like iodate, bromate, and glutaraldehyde alter cardiac sodium (Na+) channel behavior, removing inactivation and causing burst-like activity. These modified channels exhibit distinct conducting states and altered voltage-dependent kinetics.
Area of Science:
- Cardiovascular Physiology
- Ion Channel Biophysics
- Molecular Pharmacology
Background:
- Cardiac sodium channels (Na+) are crucial for heart electrical activity.
- Understanding their modulation by chemical agents is key to cardiac electrophysiology.
- Inactivation is a critical property of cardiac Na+ channels.
Purpose of the Study:
- To investigate the effects of iodate, bromate, and glutaraldehyde on single cardiac Na+ channels.
- To characterize the gating properties and kinetics of chemically modified Na+ channels.
- To explore the impact of these chemicals on Na+ channel inactivation and open states.
Main Methods:
- Recording elementary Na+ currents using cell-attached and inside-out patches.
- Applying depolarizing voltage steps to cultured neonatal rat cardiocytes.
- Analyzing single-channel activity and kinetics under chemical modification.
Main Results:
- Iodate, bromate, and glutaraldehyde removed Na+ channel inactivation.
- Modified channels displayed repetitive, burst-like activity with distinct voltage-dependent kinetics.
- Two open states were observed, with one being short-lived and voltage-independent.
- Unitary conductance remained normal (12.8 +/- 0.5 pS) despite modifications.
- Open probability declined with depolarization, and deactivation kinetics were voltage-sensitive.
Conclusions:
- Chemical modification significantly alters cardiac Na+ channel gating, primarily by removing inactivation.
- The observed burst-like activity and multiple open states suggest complex conformational changes induced by these agents.
- Modified Na+ channels exhibit unique kinetic properties distinct from normal channels and other modified channels, challenging unified models of non-inactivating channels.