Chemoreceptor and pulmonary stretch receptor interactions within amphibian respiratory control systems.

The hypercapnic drive to breathe in amphibians is generally greater than hypoxic ventilatory drive and a variety of interdependent control systems function to regulate both the hypoxic and hypercapnic ventilatory responses. During exposure to hypercapnic conditions, breathing increases in response to input from central chemoreceptors (sensitive to CSF pH/CO(2) levels) and peripheral chemoreceptors (sensitive to arterial blood O(2) and CO(2)). On the other hand, olfactory CO(2) receptors in the nasal epithelium inhibit breathing during exposure to acute hypercapnia. Further complexity arises from the CO(2)-sensitive nature of the pulmonary stretch receptors (PSR) which provide both tonic (stimulates lung inflation at low lung volumes; deflation at higher volumes) and phasic (generally excitatory) feedback. This review focuses on interactions between the various populations of chemoreceptors and interactions between chemoreceptors and PSR. Differences between various levels of experimental reduction (i.e., in vitro; in situ; in vivo) are highlighted as are the effects of chronic respiratory challenges on acute hypoxic and hypercapnic chemoreflexes.