Depletion of Ca2+ from intracellular stores potentiates spontaneous contractions of the rat portal vein

Abstract

Spontaneous contractions of the rat portal vein were potentiated in magnitude by phenylephrine, cyclopiazonic acid, ryanodine or caffeine. All these drugs can deplete Ca2+ from intracellular stores, which stimulates store-operated cation entry in some tissues. The possibility that depletion of Ca2+ from intracellular stores potentiates the spontaneous contractions was therefore investigated using functional experiments. Phenylephrine or cyclopiazonic acid was added to tissues in Ca2+-free Krebs solution, followed by a 30-min washout. After addition of extracellular Ca2+, the spontaneous contractions were potentiated. This showed the stimulus for potentiating the contractions remained so long as intracellular Ca2+ stores were depleted. Following phenylephrine washout in normal Krebs solution, potentiation of the spontaneous contractions was attenuated with time. This attenuation was abolished by the protein kinase C inhibitor calphostin C. These results show depletion of Ca2+ from intracellular stores potentiates spontaneous contractions of the portal vein. Protein kinase C may inhibit this mechanism.