POSTNATAL-DEVELOPMENT OF CO2-O-2 INTERACTION IN THE RAT CAROTID-BODY IN-VITRO

1. The effect of P-CO2 upon the discharge response to changes in P-O2 (between ca 450 and 30 mmHg) was observed in adult (> 5 weeks old) and neonatal (5-7 days old) rat carotid body chemoreceptors using an in vitro, superfused preparation. 2. In both adult and neonatal rats, regression analysis revealed that increasing P-CO2 was without effect upon the shape of the P-O2-response curves (P > 0.30), but did cause an upward shift in the position of the curves, as indicated by a significant increase in the baseline chemoreceptor discharge during hyperoxia (0.22 +/- 0.02% maximum discharge per mmHg P-CO2, P < 0.001, and 0.25 +/- 0.07% maximum discharge per mmHg P-CO2, P < 0.005, respectively). However, whilst increasing P-CO2 caused a significant rightward shift of the response curves in adults (0.75 +/- 0.23 mmHg P-O2 per mmHg P-CO2; P < 0.005), it was without effect in neonates (0.21 +/- 0.22 mmHg P-O2 per mmHg P-CO2; P < 0.200). Thus increasing levels of hypoxia increased CO2 chemosensitivity in adult but not in neonatal rats as shown by multiple regression analysis of the CO2-response curves which revealed a significant interaction between P-CO2 and P-O2 for adult (P < 0.010) but not for neonatal (P > 0.150) rats. 3. We suggest that the previously reported maturation of peripheral chemoreceptor hypoxic sensitivity (resetting) may be due to the postnatal emergence of a significant degree of interaction between P-CO2 and P-O2 at the level of the peripheral chemoreceptor and/or its afferent innervation.