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Basic FGF localization in rat carotid body: paracrine role in O2-chemoreceptor survival

Exposure of perinatal rat carotid body (CB) O2-chemoreceptors to basic fibroblast growth factor (bFGF) or hypoxia in vitro increases mitotic activity. Using double-label immunofluorescence, we localized bFGF and its receptor (FGFR) to tyrosine hydroxylase-positive (TH+) chemoreceptors in vitro; bFGF immunoreactivity also localized to chemoreceptors in CB tissue sections. Mitotic activity, measured as percentage TH+ cells that took up bromodeoxyuridine, was relatively constant (∼29%) in normoxic (20% O2) cultures grown with or without bFGF neutralizing antibody (nAb). However, the number of surviving chemoreceptors was significantly reduced in nAb-treated cultures. Under chronic hypoxia (6% O2), the presence of nAb significantly reduced chemoreceptor survival to ∼70% of control, without affecting mitotic activity. Thus, autocrine/ paracrine actions of endogenous bFGF may help promote CB chemoreceptor survival.