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

• Published in: The Journal of physiology Vol. 514; no. 2; pp. 493 - 503
• Main Authors: Wasicko, M. J., Sterni, L. M., Bamford, O. S., Montrose, M. H., Carroll, J. L.
• Format: Journal Article
• Language: English
• Published: Oxford, UK The Physiological Society 15.01.1999; Blackwell Science Ltd; Blackwell Science Inc
• Subjects: Aging - physiology; Animals; Animals, Newborn; Calcium - metabolism; Carotid Body - cytology; Carotid Body - growth & development; Carotid Body - physiology; Cell Hypoxia - physiology; Chemoreceptor Cells - cytology; Chemoreceptor Cells - drug effects; Chemoreceptor Cells - physiology; Cytosol - metabolism; Fetus; In Vitro Techniques; Original; Oxygen - pharmacology; Potassium Chloride - pharmacology; Rats
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1111/j.1469-7793.1999.493ae.x

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 [Ca 2+ ] 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 Ca 2+ -sensitive fluoroprobe fura-2. In type I cells from all age groups a graded increase in [Ca 2+ ] i occurred in response to lowering the P O 2 from 150 mmHg to 70, 35, 14, 7, 2 and 0 mmHg. The graded [Ca 2+ ] i response to hypoxia was hyperbolic at all ages. Type I cells from rats near-term fetal to 1 day old exhibited small [Ca 2+ ] i responses, mainly to the most severe levels of hypoxia. After day 1, an increase in the [Ca 2+ ] i responses to submaximal hypoxia stimulation resulted in a rightward shift in the O 2 response curve. Using the Δ[Ca 2+ ] i between 35 and 2 mmHg P O 2 as an index of O 2 sensitivity, type I cell O 2 sensitivity increased approximately 4- to 5-fold between near-term fetal to 1 day old and 11 to 14 days of age. Exposure to elevated extracellular potassium (10, 20 and 40 m m K + ) caused a dose-dependent [Ca 2+ ] i rise in type I cells from all age groups. There were no age-related changes in [Ca 2+ ] i responses to any level of K + between near-term fetal and 21 days. We conclude that the maximal type I cell [Ca 2+ ] 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 [Ca 2+ ] i response to elevated K + during the timeframe of maximal development of O 2 sensitivity suggests that resetting involves maturation of O 2 sensing, rather than non-specific developmental changes in the [Ca 2+ ] i rise resulting from depolarization.