ATP Triggers Intracellular Ca2+ Release in Type II Cells of the Rat Carotid Body

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Abstract
Using a Ca2+‐imaging technique, we studied the action of ATP on the intracellular Ca2+ concentration ([Ca2+]i) of fura‐2‐loaded mixtures of type I and type II cells dissociated from rat carotid bodies. ATP (100 μm) triggered a transient rise in [Ca2+]i in the spindle‐shaped type II (sustentacular) cells, but not the ovoid type I (glomus) cells. When challenged with ionomycin (1 μm), 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 [Ca2+]i rise was not accompanied by any current change, suggesting that P2X receptors are not involved. The ATP‐induced Ca2+ signal could be observed in the presence of Ni2+ (a blocker of voltage‐gated Ca2+ channels) or in the absence of extracellular Ca2+, indicating that Ca2+ release from intracellular stores was the dominant mechanism. The order of purinoreceptor agonist potency in triggering the [Ca2+]i rise was UTP > ATP > 2‐methylthioATP ≫α,β‐methyleneATP, implicating the involvement of P2Y2 receptors. In carotid body sections, immunofluorescence revealed localization of P2Y2 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 Ca2+ signal in type II cells can mediate paracrine interactions within the carotid bodies.