nNOS and Ca2+ influx in rat pancreatic acinar and submandibular salivary gland cells

摘要: Abstract Regulation of agonist-activated Ca 2+ influx by the NOS pathway through generation cGMP is being found in an increasing number cell types. In present work, we examined role agonist-evoked [Ca ] i oscillations and attempted to identify isoform most likely regulate influx. For this, first show that two -mobilizing agonists acting on pancreatic acinar cells, bombesin (BS) cholecystokin analog CCK-JMV-180 (CCKJ), evokes different type oscillations. The BS-evoked rapidly became acutely dependent presence extracellular , whereas CCKJ-evoked continue for long periods time absence This differential behavior allowed us isolate study its regulation while controlling non specific effects all other transporting events involved generating Inhibitors selective steps inhibited agonist-induced production. inhibitors were then used scavenging NO with reduced hemoglobin, inhibition guanylyl cyclase 1 H-[1,2,4] oxadiazolo[4,3-a] quinoxaline-1-one (ODQ) protein kinase G Rp-8-pCPT-cGMPS evoked BS but not those CCKJ. These findings extended duct cells SMG. these stimulate large influx, which was pathway. Western blot analysis immunolocalization revealed did express iNOS, eNOS expressed only blood vessels capillaries nNOS at high levels next plasma membrane cells. Accordingly, inhibitor 7-nitroindazole (7-NI) BS- into SMG Thus, together, our favor as activated released from internal stores generate