Article date: November 1987
By: Evgeny Kobrinsky, Maya Saxon in Volume 92, Issue 3, pages 499-504
The inotropic effect of a Ca2+‐entry stimulator, CGP28392, (CGP) was compared in rat and frog myocardium in a concentration‐and time‐dependent manner.
Frog preparations exhibited a persistent positive inotropic effect following prolonged treatment with CGP.
Compared to amphibian myocardium, rat ventricular muscle exhibited a biphasic time‐dependent response to CGP: an initial increase in the twitch tension amplitude of 30% was changed to a reduction of 80% below the control level during prolonged exposure to CGP (stimulation frequency, 0.2 Hz).
Following prolonged incubation with CGP, the resting‐state contraction was decreased and the negative force‐frequency relation was converted into a positive one in rat muscle.
Since sarcoplasmic reticulum (SR) is the major source of Ca2+ in a rested‐state contraction, inhibition by CGP suggests an additional, intracellular action of the Ca2+ channel activator on SR‐Ca2+ release in rat myocardium.
The inotropic effect of a Ca2+‐entry stimulator, CGP28392, (CGP) was compared in rat and frog myocardium in a concentration‐and time‐dependent manner.
Frog preparations exhibited a persistent positive inotropic effect following prolonged treatment with CGP.
Compared to amphibian myocardium, rat ventricular muscle exhibited a biphasic time‐dependent response to CGP: an initial increase in the twitch tension amplitude of 30% was changed to a reduction of 80% below the control level during prolonged exposure to CGP (stimulation frequency, 0.2 Hz).
Following prolonged incubation with CGP, the resting‐state contraction was decreased and the negative force‐frequency relation was converted into a positive one in rat muscle.
Since sarcoplasmic reticulum (SR) is the major source of Ca2+ in a rested‐state contraction, inhibition by CGP suggests an additional, intracellular action of the Ca2+ channel activator on SR‐Ca2+ release in rat myocardium.
DOI: 10.1111/j.1476-5381.1987.tb11349.x
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