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