Sodium and potassium current in neonatal rat carotid body cells following chronic in vivo hypoxia

Chronic hypoxic acclimatization modifies ventillatory reflexes arising from carotid body stimulation. To explore this, the effects of in vivo chronic hypoxia on membrane currents were quantified in chemoreceptive carotid body glomus cells. Pregnant rats were maintained in either normoxia (NORM: inspired oxygen tension 141 mmHg), or hypoxia (CHX: inspired oxygen tension 80 mmHg) from day 3 of gestation, to day 5-10 postpartum. Whole cell patch clamp recordings were then made from the mechanically and enzymatically dissociated carotid body glomus cells of the rat pups (NORM: 41 cells, CHX: 36 cells) and comparisons of means ± S.E.M. were made with unpairedt-tests. Glomus cells were bright under phase contrast illumination, formed clusters, were histochemically positive for catecholamines and possessed voltage-potassium currents that were depressed by acute hypoxia. Acclimatization to chronic hypoxia did not affect rat pup whole body mass (CHX: 12.0 ± 0.7 g vs. NORM: 11.0 ± 0.2 g), but it significantly increased blood hematocrit (CHX: 48.7 ± 0.9% vs. NORM: 37.8 ± 0.5%%,P < 0.05). Sodium current was not uniformly present in glomus cells from either group, but sodium current was observed in a greater proportion of glomus cells isolated from the chronically hypoxic pups (CHX: 72% vs. NORM: 46%,P < 0.05). The mean peak tetrodotoxin-sensitive sodium current evoked by -70 to + 10 mV depolarizations was greater after hypoxic acclimatization (CHX: -100 ± 25 vs. NORM: -38 ± 15 pA,P < 0.05), but the sodium current density (pA/pF) was unchanged. In contrast, the mean peak voltage potassium current (pA) evoked by -70 mV to 0 mV depolarizations was unchanged by acclimatization, but the potassium current density (pA/pF) was reduced (P < 0.05). Unchanged sodium current density coupled with decreased potassium current density may make glomus cells more excitable during exposure to chronic in vivo hypoxia.