Effects of Hypoxia on Cultured Chemoreceptors of the Rat Carotid Body: DNA Synthesis and Mitotic Activity in Glomus Cells

Abstract

Enlargement of the carotid body, an arterial chemosensory organ, is known to occur under natural conditions of chronic hypoxia or during hypoxic lung disease (Edwards et al 1971a,b; Dhillon et al 1984). For example, natives or animals living at high altitude (e.g. the Peruvian Andes) have enlarged carotid bodies and a high incidence of carotid body tumors (Edwards et al 1971b). This enlargement is due to both hyperplasia and hypertrophy of various cell types, including endothelial cells of the vasculature and the arterial chemoreceptors (Dhillon et al 1984; Bee et al 1986), which recent evidence indicates are the glomus or type 1 cells (Lopez-Barneo et al 1988; Biscoe and Duchen 1990; Stea and Nurse 1991 a,b). These cells are considered members of the sympathoadrenal sublineage of neural crest derivatives, and show several ultrastructural and biochemical similarities to other neuroendocrine cells of this lineage, i.e. adrenalmedullary chromaffin cells and the small intensely fluorescent (S1F) cells in sympathetic ganglia (Kobayashi 1971; McDonald and Blewett 1981; Doupe et al 1985). The mechanisms by which a simple environmental stimulus, i.e. hypoxia, triggers hyperplasia or cell division in the neuronal-like glomus cells, especially in the adult carotid body, are of general neurobiological interest since the inability of mature neurons to divide severely limits the repair capacity of the nervous system.