Chronic hypoxia abolished the postnatal increase in carotid body type I cell sensitivity to hypoxia

The O-2 sensitivity of carotid chemoreceptor type I cells is low just after birth and increases with postnatal age. Chronic hypoxia during postnatal m aturation blunts ventilatory and carotid chemoreceptor neural responses to hypoxia, but the mechanism remains unknown. We tested the hypothesis that c hronic hypoxia from birth impairs the postnatal increase in type I cell O-2 sensitivity by comparing intracellular Ca2+ concentration ([Ca2+](i)) resp onses to graded hypoxia in type I cell clusters from rats born and reared i n room air or 12% O-2. [Ca2+](i) levels at 0, 1, 5, and 21% O-2, as well as with 40 mM K+, were measured at 3, 11, and 18 days of age with use of fura 2 in freskly isolated cells. The [Ca2+](i) response to elevated CO2/low pH was measured at 11 days. Chronic hypoxia from birth abolished the normal d evelopmental increase in the type I cell [Ca2+](i) response to hypoxia. Eff ects of chronic hypoxia on development of [Ca2+](i) responses to elevated K + were small, and [Ca2+](i) responses to CO2 remained unaffected. Impairmen t of type I cell maturation was partially reversible an return to normoxic conditions. These results indicate that chronic hypoxia severely impairs th e postnatal development of carotid chemoreceptor O-2 sensitivity at the cel lular level and leaves responses to other stimuli largely intact.