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ATP Triggers Intracellular Ca 2+ Release in Type II Cells of the Rat Carotid Body
Author(s) -
Xu Jianhua,
Tse Frederick W.,
Tse Amy
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.039735
Subject(s) - extracellular , carotid body , ionomycin , intracellular , p2y receptor , chemistry , fura 2 , biophysics , depolarization , receptor , purinergic receptor , microbiology and biotechnology , cytosol , biology , endocrinology , biochemistry , stimulation , enzyme
Using a Ca 2+ ‐imaging technique, we studied the action of ATP on the intracellular Ca 2+ concentration ([Ca 2+ ] i ) of fura‐2‐loaded mixtures of type I and type II cells dissociated from rat carotid bodies. ATP (100 μ m ) triggered a transient rise in [Ca 2+ ] i in the spindle‐shaped type II (sustentacular) cells, but not the ovoid type I (glomus) cells. When challenged with ionomycin (1 μ m ), no amperometry signal could be detected from the ATP‐responsive type II cells, suggesting that these cells lacked catecholamine‐containing granules. In contrast, KCl depolarization triggered robust quantal catecholamine release from type I cells that were not responsive to ATP. In type II cells voltage clamped at −70 mV, the ATP‐induced [Ca 2+ ] i rise was not accompanied by any current change, suggesting that P2X receptors are not involved. The ATP‐induced Ca 2+ signal could be observed in the presence of Ni 2+ (a blocker of voltage‐gated Ca 2+ channels) or in the absence of extracellular Ca 2+ , indicating that Ca 2+ release from intracellular stores was the dominant mechanism. The order of purinoreceptor agonist potency in triggering the [Ca 2+ ] i rise was UTP > ATP > 2‐methylthioATP ≫α,β‐methyleneATP, implicating the involvement of P2Y 2 receptors. In carotid body sections, immunofluorescence revealed localization of P2Y 2 receptors on spindle‐shaped type II cells that partially enveloped ovoid type I cells. Since ATP is released from type I cells during hypoxia, we suggest that the ATP‐induced Ca 2+ signal in type II cells can mediate paracrine interactions within the carotid bodies.