title: Resetting and postnatal maturation of oxygen chemosensitivity in rat carotid chemoreceptor cells.
abstract: 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 PO2 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 Delta[Ca2+]i between 35 and 2 mmHg PO2 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.
authors.affiliation: Department of Pediatrics, Eudowood Division of Pediatric Respiratory Sciences, The Johns Hopkins Children's Center, Johns Hopkins School of Medicine, Baltimore MD 21287, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: Wasicko
authors.forename: L M
authors.initials: LM
authors.lastname: Sterni
authors.forename: O S
authors.initials: OS
authors.lastname: Bamford
authors.forename: M H
authors.initials: MH
authors.lastname: Montrose
authors.forename: J L
authors.initials: JL
authors.lastname: Carroll
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000378:metabolism*; D002344:Carotid Body / Q000166:cytology / Q000254:growth & development / Q000502:physiology*; D015687:Cell Hypoxia / Q000502:physiology*; D002628:Chemoreceptor Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D003600:Cytosol / Q000378:metabolism; D005333:Fetus; D066298:In Vitro Techniques; D010100:Oxygen / Q000494:pharmacology*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats
chemical_list: D011189:Potassium Chloride; D010100:Oxygen; D002118:Calcium