TY - JOUR
T1 - ATP triggers intracellular Ca2+ release in type II cells of the rat carotid body
AU - Xu, Jianhua
AU - Tse, Frederick W.
AU - Tse, Amy
PY - 2003/6/15
Y1 - 2003/6/15
N2 - 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, KCI 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.
AB - 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, KCI 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.
UR - http://www.scopus.com/inward/record.url?scp=0038380659&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0038380659&partnerID=8YFLogxK
U2 - 10.1113/jphysiol.2003.039735
DO - 10.1113/jphysiol.2003.039735
M3 - Article
C2 - 12730345
AN - SCOPUS:0038380659
SN - 0022-3751
VL - 549
SP - 739
EP - 747
JO - Journal of Physiology
JF - Journal of Physiology
IS - 3
ER -