Since glomus cell intracellular calcium ([Ca2+](i)) plays a key role in gen
erating carotid sinus nerve (CSN) discharge, we hypothesized that glomus ce
ll [Ca2+](i) would correspond to CSN discharge rates during P-O2-P-CO2 stim
ulus interaction in adult rat carotid body (CB). Accordingly, we measured s
teady state P-O2-P-CO2 interaction in CSN discharge rates during hypocapnia
(P-CO2 = 8-10 Torr), normocapnia (P-CO2 = 33-35 Torr) and hypercapnia (P-C
O2 = 68-70 Torr) in normoxia (P-O2 similar to 130 Torr) and hypoxia (P-O2 s
imilar to 36 Torr). The results showed P-O2-P-CO2 stimulus interaction in C
SN responses. [Ca2+](i) levels were measured in isolated type I cells (2-3
cells/field), using Ca2+ sensitive fluoroprobe indo-1AM. The [Ca2+](i) resp
onses increased with increasing P-CO2 normoxia. In hypoxia, [Ca2+](i) did n
ot increase during hypocapnia but increased during normocapnia, showing P-O
2-P-CO2 interaction. However, CSN response during hypoxia was far greater t
han that for [Ca2+](i) response, particularly during hypocapnic hypoxia. Th
us, the [Ca2+](i) interaction cannot account for the whole CSN interaction.
The origin of this CSN P-O2-P-CO2 interaction must have occurred in part b
eyond cellular [Ca2+](i) interaction. Interactions at both sites (glomus ce
ll membrane and sinus nerve endings) are reminiscent of reversible O-2-home
protein reaction with a Bohr effect. (C) 2000 Elsevier Science B.V. All ri
ghts reserved.