Pang L, Eyzaguirre C
Department of Physiology, University of Utah School of Medicine, Salt Lake City 84108, USA.
Biol Res. 1993;26(3):365-70.
Clusters of rat carotid body glomus cells were cultured for 1 to 12 days. Preparations were exposed to a control PO2 of 134.9 +/- 1.1 torr (mean +/- SE), and an external chloride activity, ao(Cl), of 105.6 +/- 2 mM. Thirty-six cells had a resting potential (Em) of -25.2 +/- 0.9 mV. The intracellular chloride activity, ai(Cl), was 32.8 +/- 1.1 mM, and the calculated chloride equilibrium potential (ECl) was -30.9 +/- 0.9 mV. ECl was more negative than Em, indicating that Cl- ions are not passively distributed. Hypoxia (5.4 +/- 0.8 torr), induced by Na-dithionite (Na2S2O4) 1.25 mM, elicited cell depolarization, increased ai(Cl) and a less negative ECl in about 80% of the cells. Fourteen per cent of the cells showed opposite effects. It is hypothesized that the increased ai(Cl) occurs because an outward-directed chloride pump is blocked by hypoxia. This effect is aided by depolarization of the cell. Decreased ai(Cl) may be due to cell hyperpolarization.
