Superfusion of heart cells with hyperosmotic solution causes cell shrinkage and inhibition of membrane ionic currents, including delayed-rectifer K+ currents. To determine whether osmotic shrinkage also inhibits inwardly-rectifying K+ current (I K1), guinea-pig ventricular myocytes in the perforated-patch or ruptured-patch configuration were superfused with a Tyrode’s solution whose osmolarity (T) relative to isosmotic (1T) solution was increased to 1.3–2.2T by addition of sucrose. Hyperosmotic superfusate caused a rapid shrinkage that was accompanied by a negative shift in the reversal potential of Ba2+-sensitive I K1, an increase in the amplitude of outward I K1, and a steepening of the slope of the inward I K1-voltage (V) relation. The magnitude of these effects increased with external osmolarity. To evaluate the underlying changes in chord conductance (G K1) and rectification, G K1-V data were fitted with Boltzmann functions to determine maximal G K1 (G K1max) and voltage at one-half G K1max (V 0.5). Superfusion with hyperosmotic sucrose solutions led to significant increases in G K1max (e.g., 28 ± 2% with 1.8T), and significant negative shifts in V 0.5 (e.g., −6.7 ± 0.6 mV with 1.8T). Data from myocytes investigated under hyperosmotic conditions that do not induce shrinkage indicate that G K1max and V 0.5 were insensitive to hyperosmotic stress per se but sensitive to elevation of intracellular K+. We conclude that the effects of hyperosmotic sucrose solutions on I K1 are related to shrinkage-induced concentrating of intracellular K+.
The Journal of Membrane Biology – Springer Journals
Published: Jan 1, 2004
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