Key result
Amrinone potentiated twitch amplitude and maximum tetanic tension in frog skeletal muscle fibres, enhancing the maximum contracture response to K+ by a mean of 6.3%.
Why the study?
Does amrinone alter the electromechanical coupling and contractile properties in frog skeletal muscle fibres?
Does amrinone alter the electromechanical coupling and contractile properties in frog skeletal muscle fibres?
Amrinone potentiates contractility in frog skeletal muscle fibers by reducing the mechanical threshold for depolarization-induced contracture.
Answers are grounded in this paper and cite their sources.
Amrinone's effects in frog muscle are hypothesis-generating; leaves open any cardiac relevance in mammals.
The contractile effects of 1.1 mM amrinone were studied on isolated skeletal muscle fibres of the frog (2-5 degrees C, slack length). Amrinone potentiated the twitch amplitude and the maximum tetanic tension and also enhanced the maximum contracture response elicited by 117.5 mM K+ (mean increase 6.3 +/- 1.8%, n = 6, P less than 0.02). The time to half-relaxation of the potassium contracture was slightly increased (mean change 13.8 +/- 3.5%, n = 7, P less than 0.01). Amrinone furthermore shifted the S-shaped curve relating contracture tension to log K+ to the left, and thus reduced the threshold depolarization (the mechanical threshold) needed to elicit a contracture (mean reduction 11 +/- 1 mV). The duration of the action potential at the -25 mV level was slightly increased by amrinone, whereas the resting membrane potential was unaffected.
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Mörner et al. (1990) studied Isolated skeletal muscle fibres of the frog. Amrinone was evaluated on Maximum contracture response elicited by 117.5 mM K+ (mean increase 6.3 +/- 1.8%, p=<0.02). Amrinone potentiated twitch amplitude and maximum tetanic tension in frog skeletal muscle fibres, enhancing the maximum contracture response to K+ by a mean of 6.3%.
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