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, pHo = 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-, pHo 7.15-6.85), an isohydric hypercapnia (increase in CO2 to 10% at constant pHo = 7.4) and an isocapnic acidosis (pHo = 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 pHi. The hypercapnia-induced rise of [Ca2+]i was almost completely abolished in Ca(2+)-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.
Buckler
K J
KJ
University Laboratory of Physiology, University of Oxford, UK.
Vaughan-Jones
R D
RD
D000142:Acidosis, Respiratory / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D002245:Carbon Dioxide / Q000008:administration & dosage / Q000097:blood; D002344:Carotid Body / Q000166:cytology / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D051381:Rats; D017207:Rats, Sprague-Dawley
D002245:Carbon Dioxide; D002118:Calcium