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Department of Physiology, Medical School, University of Birmingham, UK.
1. The effect of PCO2 upon the discharge response to changes in PO2 (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 PCO2 was without effect upon the shape of the PO2-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 PCO2, P < 0.001, and 0.25 +/- 0.07% maximum discharge per mmHg PCO2, P < 0.005, respectively). However, whilst increasing PCO2 caused a significant rightward shift of the response curves in adults (0.75 +/- 0.23 mmHg PO2 per mmHg PCO2; P < 0.005), it was without effect in neonates (0.21 +/- 0.22 mmHg PO2 per mmHg PCO2; 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 PCO2 and PO2 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 PCO2 and PO2 at the level of the peripheral chemoreceptor and/or its afferent innervation.
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