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Thrombin stimulates Ca-channel currents in isolated frog ventricular cells
F Markwardt1, R Albitz, T Franke
1Julius Bernstein Institute of Physiology, Martin Luther University, Halle (Saale), German Democratic Republic.
Pflugers Archiv : European Journal of Physiology
|October 1, 1988
Summary
The enzyme thrombin enhances cardiac calcium channel currents in frog heart cells, leading to positive inotropic effects. A thrombin inhibitor, hirudin, blocked this effect, confirming thrombin's role.
Area of Science:
- Cardiovascular Physiology
- Enzymology
- Cellular Electrophysiology
Background:
- Cardiac function relies on precise regulation of calcium ion (Ca2+) influx.
- Proteolytic enzymes like thrombin can influence cellular processes.
- Understanding thrombin's role in cardiac electrophysiology is crucial for cardiovascular research.
Purpose of the Study:
- To investigate the effects of thrombin on cardiac calcium channel currents.
- To determine the impact of thrombin on ventricular cell electrophysiology.
- To elucidate the mechanism behind thrombin-induced positive inotropic effects.
Main Methods:
- Utilized the whole-cell voltage clamp technique on single ventricular cells from frog myocardium.
- Applied varying concentrations of the proteolytic enzyme thrombin.
- Administered hirudin, a specific thrombin inhibitor, to assess inhibitory effects.
Main Results:
- Thrombin (3.8 x 10^-9 M) significantly increased peak Ca-channel current by 84 +/- 35% in single frog ventricular cells.
- The thrombin-induced current increase was effectively blocked by hirudin (31 x 10^-9 M).
- Observed a shift in action potential plateau voltage towards more positive values.
Conclusions:
- Thrombin modulates cardiac Ca-channel currents in frog ventricular cells.
- The observed increase in Ca-channel current by thrombin likely mediates its positive inotropic effects.
- Thrombin influences cardiac action potential characteristics, shifting plateau voltage positively.