Basic fibroblast growth factor regulates ionic currents and excitability of fetal rat carotid body chemoreceptors.

Basic fibroblast growth factor (bFGF) and nerve growth factor (NGF) are known mitogens and/or differentiation factors for cells of the sympathoadrenal lineage. Though carotid body (CB) chemoreceptors (type 1 cells) are considered part of this lineage, their response to bFGF is unknown and so far they appear unresponsive to NGF in vitro. In this study we use whole-cell recording to investigate whether bFGF (and NGF) can influence the development of ionic currents in these chemoreceptors, cultured from fetal (E18-19) rat pups. bFGF (10ng/ml) significantly augmented both transient inward Na+ and outward K+ currents in type 1 cells after only 2 days of treatment; after normalizing for the accompanying increase in cell size, as indicated by whole-cell capacitance, the Na+ current density was nonetheless increased by bFGF. Unlike controls, bFGF-treated type 1 cells readily fired action potentials following depolarization. These effects were not mimicked by NGF (100 ng/ml) treatment. Since the carotid body is one of the most richly vascularized organs and bFGF is a potent angiogenic factor, it is conceivable that variations in local bFGF concentrations during fetal development may contribute to the known species differences in CB chemoreceptor excitability.