Ventilatory sensitivity to
ammonia occurs in teleosts, elasmobranchs and mammals. Here, we investigated whether the response is also present in hagfish. Ventilatory parameters (nostril flow, pressure amplitude, velar frequency and ventilatory index, the last representing the product of pressure amplitude and frequency), together with blood and water chemistry, were measured in hagfish exposed to either high environmental
ammonia (HEA) in the external sea water or internal
ammonia loading by intra-vascular injection. HEA exposure (10 mmol l-1 NH4HCO3 or 10 mmol l-1 NH4Cl) caused a persistent
hyperventilation by 3 h, but further detailed analysis of the NH4HCO3 response showed that initially (within 5 min) there was a marked decrease in ventilation (80% reduction in ventilatory index and nostril flow), followed by a later 3-fold increase, by which time plasma total
ammonia concentration had increased 11-fold. Thus,
hyperventilation in HEA appeared to be an indirect response to internal
ammonia elevation, rather than a direct response to external
ammonia. HEA-mediated increases in oxygen consumption also occurred. Responses to NH4HCO3 were greater than those to NH4Cl, reflecting greater increases over time in water pH and PNH3 in the former. Hagfish also exhibited
hyperventilation in response to direct injection of isotonic NH4HCO3 or NH4Cl solutions into the caudal sinus. In all cases where
hyperventilation occurred, plasma total
ammonia and PNH3 levels increased significantly, while blood
acid-base status remained unchanged, indicating specific responses to internal
ammonia elevation. The sensitivity of breathing to
ammonia arose very early in vertebrate evolution.