FIGURE 2.

Schematic representation of some of adenosine cellular actions on rat carotid body (CB). Adenosine increased cAMP content in type I cells via A_2A and A_2B action on adenylyl cyclase, leading to the release of neurotransmitters, as catecholamines (Conde et al., 2008). Additionally, its action on these receptors could modulate K⁺ currents (López-López et al., 1993) for example by decreasing the amplitude of K⁺ currents (Vandier et al., 1999) and inhibit the voltage-dependent Ca²⁺ currents in type I cells. During hypoxia, adenosine released per se through the equilibrative nucleoside transport system or generated by the extracellular breakdown of ATP by 5′-ectonucleotidases (Conde and Monteiro, 2004; Conde et al., 2012a; Salman et al., 2017), acts postsynaptically on A_2A receptors, leading to adenylyl cyclase activation and to an increase in cAMP, which stimulates HCN4-containing non-selective cation channels that mediate I_h, leading to an increase in membrane excitability. In contrast, dopamine exerts the opposite effect, leading to a decrease in petrosal membrane excitability (Zhang et al., 2017).