The necessity of oxygen for survival leads to a wide variety of physiological adaptations that are induced in vertebrates during periods of low oxygen availability. Mediation of a response to hypoxia critically depends on the ability to detect decreases in oxygen supply. In mammals, peripheral oxygen chemoreceptors that can recognise decreases in arterial blood oxygen and initiate physiological responses are located within the carotid body. Fish are known to possess analogous chemoreceptors on the gill arches that mediate an increase in breathing and a decrease in heart rate during hypoxia. Fish also respond to hypoxia by releasing catecholamine hormones into the bloodstream. However, the link between detection of environmental hypoxia and this hormonal reflex remains unknown. As gill chemoreceptors elicit cardiorespiratory reflexes in fish, Stephen Reid and Steve Perry posed the hypothesis that similar branchial chemoreceptors may initiate the reflex arc,leading to catecholamine release during hypoxia in fish.
They exposed rainbow trout to sodium cyanide, either in the external water or directly into the gill circulation. Sodium cyanide is known to pharmacologically stimulate oxygen chemoreceptors. Using two methods of administration, Reid and Perry targeted externally orientated (water sensing)and internally orientated (blood sensing) chemoreceptors, to test whether either, or both, types of receptor played a role in catecholamine release. They found that there are both externally orientated and internally orientated oxygen chemoreceptors on the gills that trigger catecholamine release.
To locate these chemoreceptors, the authors repeated the administration of sodium cyanide but ligated the first gill arch. In these fish, catecholamines were still released when sodium cyanide was internally applied but not when sodium cyanide was present in the water. They concluded that externally orientated oxygen chemoreceptors are confined to the first gill arch. As catecholamine release still occurred when sodium cyanide was internally applied, internally orientated oxygen chemoreceptors appear to be located within other gill arches.
In a second part of the experiment, fish were exposed to environmental hypoxia created by bubbling nitrogen through a water–gas column. Catecholamine release occurred during environmental hypoxia even when the primary gill arch was ligated. Reid and Perry therefore conclude that internally orientated oxygen chemoreceptors are the major vector for catecholamine release during environmental hypoxia. During hypoxia, some cardiorespiratory responses occur well before catecholamines are released into the circulation and must be triggered by oxygen chemoreceptors. By measuring cardiorespiratory responses during these experiments, the authors were able to show that the oxygen chemoreceptors responsible for an increase in ventilation amplitude are distinct from those that elicit catecholamine release or a decrease in heart rate.
A lot is known about the consequences of elevated catecholamine levels during respiratory stress in fish. However, Reid and Perry are the first to identify the site of chemoreception that initiates catecholamine release during hypoxia. They have shown that peripheral oxygen receptors on the gills,orientated both externally (on the first gill arch) and internally (on all gill arches), can initiate the reflex that leads to the release of catecholamines.
