ABSTRACT

CO2 and/or pH-sensitive chemoreceptors located in the respiratory passages play an important role in ventilatory control in most vertebrates. In fish, branchial chemoreceptors appear to detect changes in water CO2 levels specifically, and are linked to the stimulation of ventilation frequency and/or amplitude, as well as to the initiation of cardiovascular responses such as bradycardia. The situation appears to be very similar for bimodal breathers (air-breathing fish and amphibian tadpoles) except that in many cases the input from these receptors is transformed with increasing levels of aquatic CO2 such that it stimulates air breathing rather than gill ventilation. CO2-sensitive chemoreceptors (gustatory and potentially, olfactory) are also located in the orobranchial cavity, although the roles of these chemoreceptors are less well understood. In air-breathing ectotherms, olfactory receptors often inhibit breathing and prolong breath holding when environmental CO2 levels are high. Pulmonary CO2/H+-sensitive receptors [intra-pulmonary chemoreceptors (IPC) and/or pulmonary stretch receptors (PSR)], on the other hand, regulate breathing pattern in all vertebrates (endotherms and ectotherms, including lungfish) in a manner that reduces dead space ventilation and enhances the efficiency of CO2 excretion under conditions of environmental hypercarbia, and/or reduces CO2 loss from hyperpnea/polypnea. This may be particularly true for IPC because of their greater CO2 sensitivity. Because there are several different CO2-sensitive chemoreceptor groups with different degrees of CO2 sensitivity eliciting different reflex responses in all vertebrates, responses to hypercarbia (elevated environmental CO2 tension) versus hypercapnia (elevated blood CO2 tension) may differ, giving rise to what appear to be anomalous responses to environmental CO2.