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

Citations Over Time

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 microM), an L-type Ca2+ channel blocker and occurred in Ca(2+)-free medium containing 50 microM EGTA. We have characterized this nicardipine-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 microM) cyclopiazonic acid (30 microM), thapsigargin (1 microM) or ryanodine (30 microM), or by incubation in Ca(2+)-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 microM) or indomethacin (10 microM) did not reduce the contraction induced by high K+. 5. Application of a protein kinase C inhibitor, H7 (10, 30 and 100 microM) or calphostin C (1 microM), 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.

Related Papers

• → Endoplasmic reticulum Ca2+ signaling and calpains mediate renal cell death(2002)54 cited
• → Thapsigargin and cyclopiazonic acid initiate rapid and dramatic increases of IL-6 mRNA expression and IL-6 secretion in murine peritoneal macrophages(1995)60 cited
• → Cyclopiazonic acid and thapsigargin induce platelet aggregation resulting from Ca2+ influx through Ca2+ store-activated Ca2+- channels(1998)11 cited
• → Modulation of cytosolic Ca2+ concentration by thapsigargin and cyclopiazonic acid in human aortic endothelial cells(1995)14 cited
• → The Ca2+-ATPase inhibitor cyclopiazonic acid and thapsigargin induces NO-mediated vasorelaxation by stimulating Ca2+ entry via receptor-operated channels.(1994)1 cited