P O 2–P CO 2 stimulus interaction in [Ca 2+] i and CSN activity in the adult rat carotid body

Abstract

Since glomus cell intracellular calcium ([Ca 2+] i) plays a key role in generating carotid sinus nerve (CSN) discharge, we hypothesized that glomus cell [Ca 2+] i would correspond to CSN discharge rates during P O 2 –P CO 2 stimulus interaction in adult rat carotid body (CB). Accordingly, we measured steady state P O 2 –P CO 2 interaction in CSN discharge rates during hypocapnia (P CO 2 =8–10 Torr), normocapnia (P CO 2 =33–35 Torr) and hypercapnia (P CO 2 =68–70 Torr) in normoxia (P O 2 ∼130 Torr) and hypoxia (P O 2 ∼36 Torr). The results showed P O 2 –P CO 2 stimulus interaction in CSN responses. [Ca 2+] i levels were measured in isolated type I cells (2–3 cells/field), using Ca 2+ sensitive fluoroprobe indo-1AM. The [Ca 2+] i responses increased with increasing P CO 2 in normoxia. In hypoxia, [Ca 2+] i did not increase during hypocapnia but increased during normocapnia, showing P O 2 –P CO 2 interaction. However, CSN response during hypoxia was far greater than that for [Ca 2+] i response, particularly during hypocapnic hypoxia. Thus, the [Ca 2+] i interaction cannot account for the whole CSN interaction. The origin of this CSN P O 2– P CO 2 interaction must have occurred in part beyond cellular [Ca 2+] i interaction. Interactions at both sites (glomus cell membrane and sinus nerve endings) are reminiscent of reversible O 2–heme protein reaction with a Bohr effect.