Sc. Hempleman, SODIUM AND POTASSIUM CURRENT IN NEONATAL RAT CAROTID-BODY CELLS FOLLOWING CHRONIC IN-VIVO HYPOXIA, Brain research, 699(1), 1995, pp. 42-50
Chronic hypoxic acclimatization modifies ventilatory reflexes arising
from carotid body stimulation. To explore this, the effects of in vivo
chronic hypoxia on membrane currents were quantified in chemoreceptiv
e carotid body glomus cells. Pregnant rats were maintained in either n
ormoxia (NORM: inspired oxygen tension 141 mmHg), or hypoxia (CHX: ins
pired oxygen tension 80 mmHg) from day 3 of gestation, to day 5-10 pos
tpartum. Whole cell patch clamp recordings were then made from the mec
hanically and enzymatically dissociated carotid body glomus cells of t
he rat pups (NORM: 41 cells, CHX: 36 cells) and comparisons of means /- S.E.M. were made with unpaired t-tests. Glomus cells were bright un
der phase contrast illumination, formed clusters, were histochemically
positive for catecholamines and possessed voltage-gated potassium cur
rents that were depressed by acute hypoxia. Acclimatization to chronic
hypoxia did not affect rat pup whole body mass (CHX: 12.0 +/- 0.7 g v
s. NORM: 11.0 +/- 0.2 g), but it significantly increased blood hematoc
rit (CHX: 48.7 +/- 0.9% vs. NORM: 37.8 +/- 0.5%, P < 0.05). Sodium cur
rent was not uniformly present in glomus cells from either group, but
sodium current was observed in a greater proportion of glomus cells is
olated from the chronically hypoxic pups (CHX: 72% vs. NORM: 46%, P <
0.05). The mean peak tetrodotoxin-sensitive sodium current evoked by -
70 mV to +10 mV depolarizations was greater after hypoxic acclimatizat
ion (CHX: -100 +/- 25 pA vs. NORM: -38 +/- 15 pA, P < 0.05), but the s
odium current density (pA/pF) was unchanged. in contrast, the mean pea
k voltage-gated potassium current (pA) evoked by -70 mV to 0 mV depola
rizations was unchanged by acclimatization, but the potassium current
density (pA/pF) was reduced (P < 0.05). Unchanged sodium current densi
ty coupled with decreased potassium current density may make glomus ce
lls more excitable during exposure to chronic in vivo hypoxia.