EFFECTS OF ACIDIC STIMULI ON INTRACELLULAR CALCIUM IN ISOLATED TYPE-I CELLS OF THE NEONATAL RAT CAROTID-BODY

We have investigated the effects of acidic stimuli upon [Ca2+](i) in isolated carotid body type I cells from the neonatal rat using indo-1 (AM-loaded). Under normocapnic, non-hypoxic conditions (23 mM HCO3-, 5% CO2 in air, pH(0) = 7.4), the mean [Ca2+](i) for single cells was 102 +/- 5.0 nM (SEM, n = 55) with 58% of cells showing sporadic [Ca2+](i) fluctuations. A hypercapnic acidosis (increase in CO2 to 10%-20% at constant HCO3-, pH(0) 7.15-6.85), an isohydric hypercapnia (increase in CO2 to 10% at constant pH(0) = 7.4) and an isocapnic acidosis (pH(0) = 7.0, constant CO2) all increased [Ca2+](i) in single cells and cell clusters. The averaged [Ca2+](i) response to both hypercapnic acidosis and isohydric hypercapnia displayed a rapid rise followed by a secondary decline. The averaged [Ca2+](i) response to isocapnic acidosis displayed a slower rise and little secondary decline. The rise of [Ca2+](i) in response to all the above stimuli can be attributed to no single factor other than to a fall of pH(i). The hypercapnia-induced rise of [Ca2+](i) was almost completely abolished in Ca2+-free solution, suggesting a role for Ca2+ influx in triggering and/or sustaining the [Ca2+](i) response. These results are consistent with a role for type I cell [Ca2+](i) in mediating pH/PCO2 chemoreception.