Abstract
Effects of intermittent (IH) and sustained hypoxia (SH) on low PO2‐evoked catecholamine (CA) secretion from neonatal rat chromaffin cells were examined. CA secretion was monitored by amperometry from chromaffin cells isolated from rat pups exposed to either IH (P0‐P5; 15s hypoxia‐5min normoxia;8h/day) or SH (hypobaric hypoxia; 0.4ATM) or normoxia (Controls). IH facilitated whereas SH attenuated hypoxia‐evoked CA secretion. IH increased the epinephrine and norepinephrine content of the adrenal medulla; whereas SH had no effect. Reactive oxygen species (ROS) levels were increased by IH but not SH. Systemic administration of MnTMPyP, a membrane permeable anti‐oxidant, prevented IH‐evoked a) facilitation of hypoxia‐induced CA secretion and b) increases in ROS as well as CA content. Elevated ROS levels and CA content persisted in P35 rats which were exposed to neonatal IH. These observations suggest that: a) neonatal IH and SH evoke diametrically opposed effects on hypoxia‐evoked CA secretion from neonatal chromaffin cells, b) ROS signaling contributes to IH but not SH evoked changes in CA secretion and c) the effects of neonatal IH on chromaffin cells persist into adult life. Supported by NIH‐HL‐76537, HL‐90554, HL‐86493 (NRP); Philip Morris USA Inc. and Philip Morris International grant (AF). D.S. is supported by fellowship from Royal Thai Government.
Published Version
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