{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T04:49:07Z","timestamp":1773290947315,"version":"3.50.1"},"reference-count":35,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2009,6]]},"abstract":"<jats:p> The objective of the present study was to examine the effects of intermittent hypoxia (IH) and sustained hypoxia (SH) on hypoxia-evoked catecholamine (CA) secretion from chromaffin cells in neonatal rats and assess the underlying mechanism(s). Experiments were performed on rat pups exposed to either IH (15-s hypoxia\/5-min normoxia; 8 h\/day) or SH (hypobaric hypoxia, 0.4 atm) or normoxia (controls) from P0 to P5. IH treatment facilitated hypoxia-evoked CA secretion and elevations in the intracellular calcium ion concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) and these responses were attenuated, but not abolished, by treatments designed to eliminate Ca<jats:sup>2+<\/jats:sup> flux into cells (Ca<jats:sup>2+<\/jats:sup>-free medium or Cd<jats:sup>2+<\/jats:sup>), indicating that intracellular Ca<jats:sup>2+<\/jats:sup> stores were augmented by IH. Norepinephrine (NE) and epinephrine (E) levels of adrenal medullae were elevated in IH-treated pups. IH treatment increased reactive oxygen species (ROS) production in adrenal medullae and antioxidant treatment prevented IH-induced facilitation of CA secretion, elevations in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> by hypoxia, and the up-regulation of NE and E. The effects of neonatal IH treatment on hypoxia-induced CA secretion and elevation in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>, CA, and ROS levels persisted in rats reared under normoxia for &gt;30 days. In striking contrast, chromaffin cells from SH-treated animals exhibited attenuated hypoxia-evoked CA secretion. In SH-treated cells hypoxia-evoked elevations in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>, NE and E contents, and ROS levels were comparable with controls. These observations demonstrate that: 1) neonatal IH and SH evoke opposite effects on hypoxia-evoked CA secretion from chromaffin cells, 2) ROS signaling mediates the faciltatory effects of IH, and 3) the effects of neonatal IH on chromaffin cells persist into adult life. <\/jats:p>","DOI":"10.1152\/jn.00036.2009","type":"journal-article","created":{"date-parts":[[2009,4,1]],"date-time":"2009-04-01T20:55:48Z","timestamp":1238619348000},"page":"2837-2846","source":"Crossref","is-referenced-by-count":49,"title":["Neonatal Intermittent Hypoxia Leads to Long-Lasting Facilitation of Acute Hypoxia-Evoked Catecholamine Secretion From Rat Chromaffin Cells"],"prefix":"10.1152","volume":"101","author":[{"given":"Dangjai","family":"Souvannakitti","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ganesh K.","family":"Kumar","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aaron","family":"Fox","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nanduri R.","family":"Prabhakar","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/j.resp.2007.09.008"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200609074"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2007.132274"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.20-14-05276.2000"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5275-05.2006"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(01)00418-4"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1038\/nature05919"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-006-0186-y"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0509844103"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2005.05.001"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00859.2005"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000101691.12358.26"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.807bs.x"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.110395"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00186.2003"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.112524"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-197708000-00007"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2009.168989"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1997.175bf.x"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1988.65.4.1796"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00644.2007"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1734109100"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00820.2003"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.114033"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2007.1732"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2004.02988.x"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.072033"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1985.sp015536"},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Seidler FJ, Slotkin TA. 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