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H 2 S Contributes to Carotid Body Response to Hypoxia but Not Anoxia
Author(s) -
Peng YingJie,
Makarenko Vladislav,
Nanduri Jayasri,
Chupikova Irina,
Girdina Anna,
Zhang Xiuli,
Kumar Ganesh,
Fox Aaron,
Prabhakar Nanduri R
Publication year - 2019
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.2019.33.1_supplement.551.14
Subject(s) - carotid body , hypoxia (environmental) , medicine , endocrinology , chemistry , stimulation , aminooxyacetic acid , sensory stimulation therapy , oxygen , biochemistry , enzyme , organic chemistry
We previously reported that cystathionine‐γ‐lyase (CSE)‐derived H 2 S mediates carotid body (CB) response to hypoxia (Hx) ( Peng et al., PNAS, 2010 ). A recent study showed that CB Type I cell responses to anoxia (Ax) were unaffected by CSE inhibitors ( Kim et al. Respir Physiology, 2015 ). We re‐examined the role of CSE‐derived H 2 S in CB sensory and Type I cell responses to Hx and Ax in adult Sprague‐Dawley rats, wild‐type and CSE knockout (KO) mice. Hx (pO 2 =37± 3mmHg) produced robust sensory excitation, and increased H 2 S levels in the CB; whereas Ax (pO 2 =5±4 mmHg) produced only a weak sensory excitation and had no effect on H 2 S levels. Ax evoked a robust [Ca 2+ ] i response of Type I cells as compared to hypoxia. CSE inhibitor DL‐propargylglycine (DL‐PAG, 50μM) inhibited Hx but not Ax‐evoked sensory and Type I responses. Higher concentration (300μM) of DL‐PAG alone, or in combination with aminooxyacetic acid (300μM), non‐selectively blocked [Ca 2+ ] i responses of Type I cells to Ax and decreased cell viability. CB sensory excitation and [Ca 2+ ] i elevation in Type I cells were unaffected in CSE null mice as compared to wild‐type (Wt) mice. Breathing stimulation by Hx was absent in CSE KO mice, whereas depressed breathing by Ax was unaffected. These observations suggest that CSE‐derived H 2 S contributes to carotid body response to “physiologically” relevant hypoxia but not to anoxia. Support or Funding Information Supported by National Institutes of Health grants P01‐HL‐90554 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .