Sensitivity to protein kinase C inhibitors of nicardipine‐insensitive component of high K+ contracture in rat and guinea‐pig aorta

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Abstract
1 In the rat and guinea-pig aorta, we observed that the contraction to hypertonically-added K+, unlike the isotonic K+-induced contraction, was only partially sensitive to nicardipine (0.1, 1 and 10 μm), an L-type Ca2+ channel blocker and occurred in Ca2+-free medium containing 50 μm EGTA. We have characterized this nicarpidine-insensitive hypertonically-added K+ contraction. 2 The contraction induced by an equi-osmolar concentration of mannitol was similar in size to that evoked by hypertonically-added K+. 3 When the tissue was depleted of its internal Ca2+ stores with various agents such as phenylephrine (10 μm), cyclopiazonic acid (30 μm), thapsigargin (1 μm) or ryanodine (30 μm), or by incubation in Ca2+-free medium over 30 min, little effect was observed on the high K+ contracture in the presence of L-type Ca2+ channel blockade. 4 Phentolamine (10 μm) or indomethacin (10 μm) did not reduce the contraction induced by high K+. 5 Application of a protein kinase C inhibitor, H7 (10, 30 and 100 μm) or calphostin C (1 μm), reduced the high K+ contraction but not that caused by an equi-osmolar concentration of mannitol. 6 The data suggest that hypertonic K+-induced contraction differs from that caused by hypertonicity or depolarization per se and invokes membrane enzyme activation.

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