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H 2 S MEDIATES SENSORY LONG‐TERM FACILITATION OF THE CAROTID BODY
Author(s) -
Peng YingJie,
Yuan Guoxiang,
Khan Shakil,
Nanduri Jayasri,
Kumar Ganesh,
Snyder Solomon,
Prabhakar Nanduri
Publication year - 2017
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.31.1_supplement.1024.3
Subject(s) - carotid body , endocrinology , medicine , hypoxia (environmental) , intermittent hypoxia , obstructive sleep apnea , sensory system , facilitation , chemistry , biology , stimulation , neuroscience , organic chemistry , oxygen
Chronic intermittent hypoxia (CIH) is a hallmark manifestation of sleep apnea. Rodents treated with CIH exhibit hypertension and increased sympathetic nerve activity, and these effects were attributed to carotid body (CB) chemoreflex. CIH leads to CB activation manifested by augmented sensory response to hypoxia, and sensory long‐term facilitation (LTF). The purpose of the present study is to determine the mechanisms underlying CB activation by CIH. Recent studies suggest that the gasotransmitter H 2 S mediates CB activation during acute hypoxia. Since CIH increases H 2 S production from the cystathionine‐ϒ‐lyase (CSE) in the CB through ROS signaling, we hypothesized that H 2 S mediates the CB activation by CIH. Experiments were performed on adult rats, CSE‐null and wild‐type mice treated with 10 days of CIH. CIH treated CBs displayed augmented sensory response to hypoxia, and sensory LTF in rats and wild‐type mice. CB activation by CIH was completely absent in rats treated with L‐Propargylglycine (L‐PAG) an inhibitor of CSE and in mice deficient in CSE. CIH treated rats and wild‐type mice showed hypertension, increased sympathetic nerve activity, and elevated plasma catecholamine levels ‐ all these effects were remarkably absent in L‐PAG treated rats and CSE null mice. These findings suggest that ROS‐dependent activation of CSE‐derived H 2 S synthesis mediates CB response to CIH and the ensuing hyperactive CB chemoreflex contributes to CIH‐induced sympathetic activation and hypertension. Support or Funding Information Supported by NIH‐PO1‐HL90554