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ATP inhibits the hypoxia response in type I cells of rat carotid bodies
Author(s) -
Xu Jianhua,
Xu Fenglian,
Tse Frederick W.,
Tse Amy
Publication year - 2005
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2004.02978.x
Subject(s) - carotid body , hypoxia (environmental) , chemistry , microbiology and biotechnology , medicine , endocrinology , biology , biochemistry , neuroscience , electrophysiology , oxygen , organic chemistry
Summary During hypoxia, ATP was released from type I (glomus) cells in the carotid bodies. We studied the action of ATP on the intracellular Ca 2+ concentration ([Ca 2+ ] i ) of type I cells dissociated from rat carotid bodies using a Ca 2+ imaging technique. ATP did not affect the resting [Ca 2+ ] i but strongly suppressed the hypoxia‐induced [Ca 2+ ] i elevations in type I cells. The order of purinoreceptor agonist potency in inhibiting the hypoxia response was 2‐methylthioATP > ATP > ADP ≫ α, β‐methylene ATP > UTP, implicating the involvement of P2Y 1 receptors. Simultaneous measurements of membrane potential and [Ca 2+ ] i show that ATP inhibited the hypoxia‐induced Ca 2+ signal by reversing the hypoxia‐triggered depolarization. However, ATP did not oppose the hypoxia‐mediated inhibition of the oxygen‐sensitive TASK‐like K + background current. Neither the inhibition of the large‐conductance Ca 2+ ‐activated K + (maxi‐K) channels nor the removal of extracellular Na + could affect the inhibitory action of ATP. Under normoxic condition, ATP caused hyperpolarization and increase in cell input resistance. These results suggest that the inhibitory action of ATP is mediated via the closure of background conductance(s) other than the TASK‐like K + , maxi‐K or Na + channels. In summary, ATP exerts strong negative feedback regulation on hypoxia signaling in rat carotid type I cells.