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ATP triggers intracellular Ca²⁺ release in type II cells of the rat carotid body

Jianhua Xu, Frederick W. Tse and Amy Tse

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 >> ,-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.

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