Aim: 

Hypoxia produces carotid body chemoreceptor cells (CBCC) activation leading to neurotransmitter release, augmented sinus nerve activity and subsequent ventilatory and cardiovascular reflexes and thereby the recovery of arterial oxygenation. Hypoxia is known to produce an increase of calcium influx via voltage dependent-Ca²⁺ channels, leading to the neurotransmitters release, mainly catecholamines. Recovery of calcium levels after stimulation has not yet been studied in this cell type. Plasma membrane Ca²⁺-ATPase and the Na/Ca exchanger (NCX) are the main Ca²⁺ efflux pathways from cells. Although the primary role of NCX is to extrude Ca²⁺ from cells, it may also mediate Ca²⁺ influx when NCX is working in reverse mode. We aim to characterize the presence and significance of NCX in Ca²⁺ homeostasis in these cells.

Methods: 

We have monitored [Ca]_i changes by Fura-2 fluorescence in isolated cells and analyzed the exocytotic release of [³H]-catecholamines in whole carotid bodies.

Results and Conclusion: 

Exposure of cells to Na⁺-free solution caused a rise in [Ca²⁺]_i promoting catecholamine secretion, consistent with Ca²⁺ entry through NCX. These effects were inhibited to various levels by application of 5 mM Ni²⁺ or 10 mM KB-R7943, two well known NCX inhibitors. In Na-free solution the hypoxia-induced catecholamine release was reduced by 95% whereas high K⁺-induced release was enhanced. This effect demonstrates NCX participation in Ca²⁺ homeostasis in basal and stimulated CBCC. Finally, by RT-PCR we have assessed the expression of NCX mRNA in CBCC.

Supported by grants BFU2005-05464, BFU2007-61848 (DGICYT), SAN673-VA12/08 and VA104A08 (JCyL)