Resetting and postnatal maturation of oxygen chemosensitivity in rat carotid chemoreceptor cells

1. Carotid chemoreceptor sensitivity is minimal immediately after birth and increases with postnatal age. In the present study we have investigated th e peri- and postnatal developmental time course of [Ca2+](i) responses to h ypoxia in clusters of type I cells isolated from near-term fetal rats and r ats that were 1, 3, 7, 11, 14 and 21 days old, using the Ca2+-sensitive flu oroprobe fura-2. 2. In type I cells from all age groups a graded increase in [Ca2+](i) occur red in response to lowering the P-O2 from 150 mmHg to 70, 35, 14, 7, 2 and 0 mmHg. The graded [Ca2+](i) response to hypoxia was hyperbolic at all ages . 3. Type I cells from rats near-term fetal to 1 day old exhibited small [Ca2 +](i) responses, mainly to the most severe levels of hypoxia. After day 1, an increase in the [Ca2+](i) responses to submaximal hypoxia stimulation re sulted in a rightward shift in the 0, response curve. Using the Delta[Ca2+] (i) between 35 and 2 mmHg P-O2 as an index of O-2 sensitivity, type I cell O-2 sensitivity increased approximately 4- to 5-fold between near-term feta l to 1 day old and 11 to 14 days of age. 4. Exposure to elevated extracellular potassium (10, 20 and 40 mM K+) cause d a dose-dependent [Ca2+](i) rise in type I cells from all age groups. Ther e were no age-related changes in [Ca2+](i) responses to any level of K+ bet ween near-term fetal and 21 days. 5. We conclude that the maximal type I cell [Ca2+](i) response to anoxia, a s well as the sensitivity to submaximal hypoxic stimulation, of rats aged f rom near-term fetal to 21 days depends on the level of postnatal maturity. The lack of an age-related increase in the [Ca2+](i) response to elevated K + during the timeframe of maximal development of O-2 sensitivity suggests t hat resetting involves maturation of O-2 sensing, rather than non-specific developmental changes in the [Ca2+](i) rise resulting from depolarization.