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Hypoxia evokes catecholamine secretion from rat pheochromocytoma PC-12 cells.

Abstract
We have monitored exocytosis of catecholamines from individual PC-12 cells by amperometry using carbon fiber microelectrodes in order to investigate possible secretory responses to acute hypoxia. In normoxia, no secretion was detected from cells perfused with a solution containing 5 mM K+. However, when [K+] was raised (10-100 mM), exocytotic events were observed. Hypoxia (PO2 11 mmHg) stimulated secretion from PC-12 cells, and in hypoxic conditions exocytosis was greater at each [K+] studied as compared with normoxia. Hypoxia-evoked secretion was abolished in Ca2+ free solutions containing 1 mM EGTA and by the non-specific Ca2+ channel blocker, Cd2+ (200 microM). Secretion was also largely inhibited by omega-conotoxin GVIA (1 microM). Exocytosis was also observed in normoxia when cells were exposed to tetraethylammonium (1-10 mM), but not 4-aminopyridine (3 mM). Our findings indicate that hypoxia evokes exocytosis via depolarization arising from inhibition of a TEA-sensitive K+ conductance, leading to Ca2+ influx primarily via N-type Ca2+ channels.
AuthorsS C Taylor, C Peers
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 248 Issue 1 Pg. 13-7 (Jul 09 1998) ISSN: 0006-291X [Print] United States
PMID9675077 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Calcium Channel Blockers
  • Calcium Channels
  • Catecholamines
  • Peptides
  • Spider Venoms
  • omega-Agatoxin IVA
  • Cadmium
  • Tetraethylammonium
  • omega-Conotoxin GVIA
  • Nifedipine
  • Potassium
  • Calcium
Topics
  • Animals
  • Cadmium (pharmacology)
  • Calcium (metabolism)
  • Calcium Channel Blockers (pharmacology)
  • Calcium Channels (drug effects, metabolism)
  • Catecholamines (metabolism)
  • Cell Hypoxia (physiology)
  • Exocytosis (drug effects)
  • Nifedipine (pharmacology)
  • PC12 Cells
  • Peptides (pharmacology)
  • Potassium (metabolism)
  • Rats
  • Spider Venoms (pharmacology)
  • Tetraethylammonium (pharmacology)
  • omega-Agatoxin IVA
  • omega-Conotoxin GVIA

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