Increased Intracellular Potassium and Water Contents in Rat Heart after α‐1‐Adrenoceptor Stimulation

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Abstract
Potassium accumulation in rat heart after α‐1‐adrenoceptor stimulation has previously been reported from indirect measurements. Here we present data on intracellular potassium content measured directly in the heart. Isolated rat hearts perfused in a non‐recirculating system were exposed to α‐1‐adrenoceptor stimulation (5 × 10‐5mol/1 phenylephrine in the presence of 10−6mol/1 timolol).14C‐Sucrose was used to estimate the extracellular space. From heart homogenates intracellular potassium, magnesium and cellular water contents were determined and the ion concentrations calculated accordingly. The intracellular magnesium content remained unchanged during all experimental conditions. α‐1‐Adreno‐ceptor stimulation evoked an increase in potassium content by 9% (4, 14; 95% confidence interval (CI), P=0.0006). Due to an observed increase in intracellular water by 17% (9, 26; 95% CI, P=0.0006), the potassium concentration apparently decreased by 8% (0.3, 15; 95% CI, P=0.04). During partial inhibition of the Na+/K+‐ATPase by 10−5mol/1 ouabain, there was an increase in potassium content by 5% (1, 9; 95% CI, P=0.008). There was, however, no significant increase in intracellular water in this situation. Calculated intracellular potassium concentration showed accordingly a slight increase. The effects upon potassium and water both in the absence and presence of ouabain were eliminated by the α‐1‐adrenocep‐tor blocker prazosin (10−6 mol/1). α‐1‐Adrenoceptor stimulation apparently increased cellular dry weight by 10% (2, 18; 95% CI, P=0.02). Changes in translocation of potassium and water must be considered as part of the α‐1‐adrenergic heart effects.