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H2S generated by Cystathionine γ‐lyase Mediates Hypoxia‐evoked Catecholamine Secretion from Neonatal Adrenal Medullary Chromaffin cells
Author(s) -
Souvannakitti Dangjai,
Nanduri Jayasri,
Fox Aaron P,
Gadalla Moataz M,
Kumar Ganesh K,
Snyder Solomon,
Prabhakar Nanduri
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.669.20
Neonatal adrenal medullary chromaffin cells (AMC) are extremely sensitive to hypoxia, and low O 2 stimulates catecholamine secretion. Given that H 2 S generated by cystathionine γ‐lyase (CSE) is important for mediating carotid body responses to hypoxia, we examined whether hypoxia‐evoked catecholamine secretion from neonatal AMC requires similar signaling mechanisms. Experiments were performed on rats and mice aged P10. Catecholamine secretion was monitored by amperometry using a carbon fiber electrode. AMC from rats and mice expressed CSE‐like immunoreactivity. Genetic deletion of CSE markedly impaired hypoxia‐evoked catecholamine secretion from mice AMC; whereas high potassium‐evoked catecholamine secretion was unaffected. Similar impairment of low O 2 ‐evoked but not high K + induced catecholamine secretion was seen in rat AMC treated with the CSE inhibitor, DL‐propargyl glycine (DL‐PAG; 30–50 μM). These results demonstrate that like in the carotid body, H 2 S derived from CSE mediates hypoxic sensing by neonatal AMC. Supported by HL‐90554, HL‐76537, HL‐86493 and HL‐089616.