Increases in extracellular K(+) concentrations reduced the twitch force amplitude of heart muscle from the freshwater turtle (Trachemys scripta elegans) and rainbow trout (Oncorhynchus mykiss). Adrenaline augmented twitch force amplitude and reduced the relative influence of [K(+)]. In the absence of adrenaline, high [K(+)] had less effect in reducing twitch force in turtle than in trout, whereas the reverse was true in the presence of adrenaline. Under anoxic conditions, twitch force was lower in 10 mmol l(−1) than in 2.5 mmol l(−1) K(+) in both preparations, but adrenaline removed this difference. A further analysis of turtle myocardium showed that action potential duration was shorter and resting potential more positive in high [K(+)] than in low [K(+)]. Adrenaline restored the duration of the action potential, but did not affect the depolarisation, which may attenuate Na(+)/Ca(2+) exchange, participating in excitation/contraction coupling. The contractile responses in the presence of adrenaline were, however, similar in both high and low K(+) concentrations when increases in extracellular Ca(2+) were applied to increase the demand on excitation/contraction coupling. The possibilities that adrenaline counteracts the effects of high [K(+)] via the sarcoplasmic reticulum or sarcolemmal Na(+)/K(+)-ATPase were examined by inhibiting the sarcoplasmic reticulum with ryanodine (10 micromol l(−1)) or Na(+)/K(+)-ATPase with ouabain (0.25 or 3 mmol l(−)). No evidence to support either of these possibilities was found. Adrenaline did not protect all aspects of excitation/contraction coupling because the maximal frequency giving regular twitches was lower at 10 mmol l(−1) K(+) than at 2.5 mmol l(−1) K(+).

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