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Carotid body response to intermittent hypoxia requires Ca v 3.2 T‐type Ca 2+ channels
Author(s) -
Makarenko Vladislav,
Nanduri Jayasri,
Fox Aaron,
Kumar Ganesh,
Prabhakar Nanduri
Publication year - 2015
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.29.1_supplement.681.2
Subject(s) - glomus cell , carotid body , hypoxia (environmental) , endocrinology , chemistry , intermittent hypoxia , medicine , chemoreceptor , receptor , biology , stimulation , oxygen , organic chemistry , obstructive sleep apnea
Previous studies showed that intermittent hypoxia (IH) augments carotid body response to hypoxia, but the underlying cellular mechanisms are not known. We recently reported that carotid body glomus cells express α 1H subunit of Ca v 3.2 T‐type Ca 2+ channels, which contribute to hypoxia‐evoked Ca 2+ influx. In the present study we examined the role of Ca v 3.2 in glomus cell responses to IH. Carotid bodies from IH exposed rats exhibited 3 fold increase in α 1H mRNA as compared with control rats reared under normoxia. IH exposed glomus cells exhibited augmented [Ca 2+ ] i response to acute hypoxia. TTA‐A2 (25 µM), a selective blocker of T‐type Ca 2+ channels, attenuated hypoxia‐evoked [Ca 2+ ] i elevation in by ~45% in controls and by ~80% in IH‐exposed glomus cells. The IH‐evoked augmented [Ca 2+ ] i responses to acute hypoxia was absent in α 1H null glomus cells. These results demonstrate that Ca v 3.2 T‐type Ca 2+ channels contribute to IH‐induced augmented [Ca 2+ ] i responses in glomus cells. Supported by NIH HL‐90554.