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Hydrogen sulfide mediates catecholamine secretion elicited by hypoxia in the carotid body
Author(s) -
Makarenko Vladislav,
Peng Ying-Ji,
Nanduri Jayasri,
Snyder Solomon H.,
Fox Aaron P.,
Prabhakar Nanduri R.
Publication year - 2012
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.26.1_supplement.897.8
Subject(s) - glomus cell , carotid body , hypoxia (environmental) , secretion , endocrinology , medicine , catecholamine , chemistry , biology , oxygen , stimulation , organic chemistry
We previously demonstrated that H 2 S is a physiologic transmitter in the carotid body, enhancing responses to hypoxia. Carotid bodies express the H 2 S producing enzyme cystathionine γ‐lyase (CSE). Genetic ablation of CSE or inhibition by DL‐propargylglycine (PAG) eliminated carotid body sensory and ventilatory responses to hypoxia. In the present study we examine the role of H 2 S in the glomus cell's response to hypoxia. Catecholamine secretion was monitored by carbon fiber amperometry and [Ca 2+ ] i with fura 2. In rat glomus cells PAG attenuated the secretory response to hypoxia, but did not alter secretion elicited by high‐K + . Experiments with CSE −/− mice produced similar results; glomus cells from CSE −/− mice showed little catecholamine secretion in response to hypoxia, but exhibited robust secretion when exposed to high‐K + . Secretion is tightly regulated by [Ca 2+ ] i . PAG treated rat glomus cells exhibited reduced elevation of [Ca 2+ ] i in response to hypoxia. Exposing rat glomus cells to the H 2 S donor NaHS produced an elevation in [Ca 2+ ] i that mimicked the elevation of [Ca 2+ ] i elicited by hypoxia. More importantly, glomus cells from CSE −/− mice had markedly attenuated elevation of [Ca 2+ ] i in response to hypoxia. These results suggest that hypoxia evoked catecholamine secretion from glomus cells is mediated by H 2 S via a Ca 2+ dependent mechanism. Supported by NIH HL‐90554, HL‐86493.