AbstractWe designed the present study to determine whether Ca2+release from intracellular stores contributes to flow-induced contraction. We carried out experiments on segments of rabbit facial vein under isometric conditions. Intraluminal flow by perfusion of physiological salt solution (10 to 80 μL/min) caused contraction in this vessel, which was significantly inhibited by (1) 30-minute pretreatment with 10 μmol/L ryanodine, the sarcoplasmic reticulum Ca2+channel opener, and (2) 30-minute pretreatment with concomitant application of 20 mmol/L caffeine and 1 μmol/L cyclopiazonic acid in Ca2+-free medium to deplete the sarcoplasmic reticulum. In comparison, contraction initiated by 300 nmol/L histamine was significantly attenuated by the same interventions. K+(25 mmol/L)–induced contraction was unaffected by ryanodine but was reduced after depletion of the sarcoplasmic reticulum. The phospholipase C inhibitor 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (10 μmol/L) inhibited contractions induced by flow and histamine but not by K+. These findings indicate that Ca2+release from intracellular stores, presumably via the phosphatidylinositol pathway, contributes to flow- and histamine- but not raised K+–induced contractions in this vessel.