1. Carotid chemoreceptor sensitivity is minimal immediately after birth and increases with postnatal age. In the present study we have investigated the peri- and postnatal developmental time course of [Ca2+](i) responses to hypoxia in clusters of type I cells isolated from near-term fetal rats and rats that were 1, 3, 7, 11, 14 and 21 days old, using the Ca2+ sensitive fluoroprobe fura-2. 2. In type I cells from all age groups a graded increase in [Ca2+](i) occurred 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 resulted in a rightward shift in the O2 response curve. Using the Δ[Ca2+](i) between 35 and 2 mmHg P(O2) as an index of O2 sensitivity, type I cell O2 sensitivity increased approximately 4- to 5-fold between near-term fetal to 1 day old and 11 to 14 days of age. 4. Exposure to elevated extracellular potassium (10, 20 and 40 mm K+) caused a dose-dependent [Ca2+](i) rise in type I cells from all age groups. There were no age-related changes in [Ca2+](i) responses to any level of K+ between near term fetal and 21 days. 5. We conclude that the maximal type I cell [Ca2+](i) response to anoxia, as well as the sensitivity to submaximal hypoxic stimulation, of rats aged from 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 O2 sensitivity suggests that resetting involves maturation of O2 sensing, rather than non-specific developmental changes in the [Ca2+](i) rise resulting from depolarization.
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