Key result
4-Aminopyridine induced contracture in frog heart ventricular strips even under full mechanical inhibition, indicating calcium release from the sarcoplasmic reticulum.
4-Aminopyridine can induce calcium release from internal stores (sarcoplasmic reticulum) in frog heart ventricular strips, which may be important for its cardiac actions.
No immediate clinical implications; hypothesis-generating for SR calcium release mechanisms in amphibian cardiac tissue.
4-Aminopyridine (4-AP), a K(+)-channel blocker, has been associated with cellular Ca2+ movements in various excitable tissues but its interaction with intracellular Ca2+ pools has not been described. Spontaneously beating ventricular strips of frog hearts responded to 4-AP (1.6 x 10(-2) M) by contracture that was susceptible to tolerance development when 4-AP was applied in a repetitive manner after washout periods. Under full mechanical inhibition by Ca(2+)-free Ringer or high-K+ Ringer or a combination of both, 4-AP could still produce contracture, a finding indicating that the source of Ca2+ for such an effect should be intracellular Ca2+ pools, namely the sarcoplasmic reticulum. It was concluded that 4-AP could induce release of Ca2+ from internal stores that might be of importance in its cardiac actions.
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Sılan et al. (2000) studied this question. 4-Aminopyridine (4-AP) was evaluated on Contracture. 4-Aminopyridine induced contracture in frog heart ventricular strips even under full mechanical inhibition, indicating calcium release from the sarcoplasmic reticulum.
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