Does Catecholamine Secretion Mediate the Hypoxia-lnduced Increase in Nerve Activity?

Abstract

Catecholamine secretion from carotid body glomus cells is hypothesized to cause the hypoxia-induced increase in nerve activity. To test aspects of this hypothesis, tissue catecholamine and single-fiber nerve activity was measured from rat carotid bodies in vitro. Hypoxia (1-min duration, 0 Torr at nadir) caused a rapid increase in catecholamine release and nerve activity, consistent with the hypothesis, but repetitive hypoxias interspersed with short rest periods resulted in a much greater decline in catecholamine release than nerve activity. Furthermore, pretreatment with reserpine (24 h) nearly abolished catecholamine release, but nerve response was not different than untreated controls. These results suggest that catecholamine secretion is not causal to the increase in nerve activity of rat carotid body.

Synapse Formation and Hypoxic Signalling in Co‐Cultures of Rat Petrosal Neurones and Carotid Body Type 1 Cells

“…PNs without obvious changes in firing threshold ( n = 12; not shown). Taken together, these data argue that ACh, rather than dopamine, is probably a major excitatory neurotransmitter during hypoxic signalling in the rat CB (see also Donnelly, 1995). However, in a few experiments ( n = 4) high concentrations of hexamethonium (200/*m) were insufficient to block completely the hypoxia‐induced depolarization, although action potentials were abolished.…”

“…The excitatory neurotransmitter that mediates afferent discharge in the CB during hypoxia remains controversial (Gonzalez et al 1994; Fitzgerald & Shirahata, 1994; Donnelly, 1995). Since dopamine is the best studied neurotransmitter in the CB, and its release from type 1 cells is well correlated with hypoxic stimulation (Gonzalez et al 1994), we tested whether perfusion of the D 2 receptor blocker spiperone (10–50 μm), significantly affected the hypoxia‐induced chemosensory discharge in co‐culture.…”

“…In a few experiments, the dopamine D 2 receptor blocker, spiperone (10–50 μ m ) had no appreciable effect on the hypoxic discharge in functional co‐cultured PNs. The role of dopamine in CB chemotransmission remains controversial (see Gonzalez et al 1994), although other recent studies suggest it is unlikely to be the mediator of hypoxic signalling in the mammalian CB (Donnelly, 1995; Iturriaga, Alcayaga & Zapata, 1996).…”

Angiotensin AT1 receptor‐mediated excitation of rat carotid body chemoreceptor afferent activity

“…This association includes dopaminergic neurons in the brain, with AngII acting presynaptically in the striatum to potentiate dopamine release (Mendelsohn, Jenkins & Berkovic, 1993). Whilst the role of dopamine in the carotid body remains controversial, it has been proposed that dopamine release from glomus cells acts on chemoreceptor afferent terminals to increase activity (Gonzalez, LopezLopez, Obeso, Perez-Garcia & Rocher, 1995;Donnelly, 1995). Given the precedent of AngII modulating dopamine release in the central nervous system, it is possible that potentiation of the release of dopamine from glomus cells might mediate the excitatory effect of AngII.…”

Neurotransmission in the carotid body and anesthesia

“…Modified from Igarashi et al [ ). Dissociation between catecholamine release and chemoreceptor neural response has also been reported [122][123][124]. Based on all the data, the generally accepted current understanding is that dopamine is an inhibitory neurotransmitter in the carotid body.…”