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Ca-channel currents in isolated frog ventricular cells are increased by thrombin
R Albitz1, F Markwardt, T Franke
1Julius Bernstein Institute of Physiology, Martin Luther University, Halle, GDR.
Biomedica Biochimica Acta
|January 1, 1989
Summary
Thrombin, a cardiac enzyme, significantly boosts calcium channel currents in frog heart cells. This effect, blocked by the inhibitor hirudin, explains thrombin's positive inotropic impact on the frog heart.
Area of Science:
- Cardiovascular Physiology
- Enzymology
- Molecular Cardiology
Background:
- Thrombin is a serine protease with known roles in coagulation.
- Its direct effects on cardiac ion channels are not fully elucidated.
- Understanding enzyme-channel interactions is crucial for cardiac function research.
Purpose of the Study:
- To investigate the impact of thrombin on cardiac calcium channel currents.
- To determine if thrombin modulates ion channel activity in ventricular cells.
- To correlate these effects with observed physiological responses in the heart.
Main Methods:
- Utilized the whole-cell voltage clamp technique on isolated frog ventricular cells.
- Applied specific concentrations of thrombin to the cell bath.
- Administered hirudin, a specific thrombin inhibitor, to assess specificity.
Main Results:
- Thrombin (3.8 x 10(-9) M) significantly increased peak Ca-channel current by 84% +/- 35% in 8 cells.
- The thrombin-induced current increase was fully blocked by hirudin.
- This modulation suggests a direct enzymatic effect on calcium channels.
Conclusions:
- Thrombin directly modulates cardiac calcium channel currents in frog myocardium.
- This modulation is responsible for the positive inotropic effects of thrombin on the frog heart.
- Findings highlight a novel role for thrombin in cardiac electrophysiology.