Abstract
Intrapulmonary chemoreceptors (IPC) are neurons that sense tonic and phasic CO2 stimuli in the lungs of birds and diapsid reptiles. IPC are different from most other vertebrate respiratory CO2 receptors because: (1) they are stimulated by low PCO2 and inhibited by high PCO2, (2) they have extremely rapid response characteristics, (3) their CO2 sensitivity is nearly abolished by intracellular inhibitors of carbonic anhydrase, and (4) their CO2 sensitivity is strongly depressed by inhibiting Na+/H+ antiport exchange. Experimental evidence suggests that IPC respond to intracellular pH, not CO2 directly, and that intracellular pH and IPC discharge are determined by a kinetic balance between CO2 hydration/dehydration rates, transmembrane acid/base exchange rates, and intracellular buffering. We review experimental evidence for and against various mechanisms of IPC CO2 chemotransduction, present a conceptual and mathematical model of the proposed mechanisms, and compare this model to CO2 transduction in other respiratory chemoreceptors.
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