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

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 mum) 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 mum), 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 much greater than alpha,beta-methyIeneATP, 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 Ca2+ signal in type II cells can mediate paracrine interactions within the carotid bodies.