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J Biol Chem, Vol. 274, Issue 44, 31217-31222, October 29, 1999

Hypoxic Enhancement of Quantal Catecholamine Secretion
EVIDENCE FOR THE INVOLVEMENT OF AMYLOID -PEPTIDES

From the Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT, United Kingdom

Prolonged exposure to hypoxia (10% O₂) enhanced quantal catecholamine release evoked from O₂-sensing pheochromocytoma (PC12) cells, as monitored using single-cell amperometric recordings. The enhancement of exocytosis was apparent after 12 h of hypoxia and was maximal at 24 h. Elevated levels of secretion were due to the emergence of a Ca²⁺ influx pathway that persisted during complete blockade of known voltage-gated Ca²⁺ channels. Secretion triggered by this Ca²⁺ influx was severely reduced by known inhibitors of Alzheimer's amyloid -peptides (APs), including an N terminus-directed monoclonal antibody. The enhancing effect on secretion of chronic hypoxia was mimicked closely by direct application of AP to cells under normoxic conditions, although the effects of AP were more rapid at onset, being maximal after only 6 h. The present results suggest that prolonged hypoxia can induce formation of Ca²⁺-permeable AP channels and that such induction can lead directly to excessive neurosecretion. This is a potential contributory factor to AP pathophysiology following cerebral ischemia.

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