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Oxygen-sensitive chemoreceptors and cardiovascular and ventilatory control in rainbow trout

University of British Columbia

Fish respond to changes in external (water) and internal (blood/tissue) O₂ levels by altering cardiovascular and ventilatory performance. These reflexes are mediated, for the most part, by O₂-sensitive chemoreceptors. Although the reflex responses of intact fishes have been characterized in detail, the receptors mediating these reflexes to hypoxia are poorly understood. To this end, afferent neural activity from O₂-sensitive chemoreceptors was recorded from the glossopharyngeal nerve (cranial nerve IX) in the isolated, perfused first gill arches of rainbow trout (Oncorhynchus mykiss). Branchial O₂-sensitive chemoreceptors were sensitive to changes in external and/or internal O₂ tensions. Some receptors were sensitive to either internal or external O₂ levels and others were sensitive to both. External receptors showed an increase in activity as the PO₂ was decreased to about 40 torr. Below 40 torr, afferent activity was depressed but recovered as P₀₂s was increased. Reversible depression of O₂ receptor activity at low P₀₂s has been observed in mammalian O₂ receptors and is believed to illustrate the dependence of receptor activity on oxidative metabolism (Lahiri et al., 1983). Occluding perfusate flow through the gill had little effect on afferent activity indicating that the internal receptors were not very flow sensitive. Sodium cyanide, a potent O₂ receptor stimulant, dramatically increased afferent neural activity. The response characteristics of these receptors are similar to tuna gill and mammalian carotid body O₂ receptors and suggest that these may be the receptors that mediate the cardiovascular and ventilatory reflex responses of fishes to hypoxia. A number of different neurochemicals are thought be involved in O₂ transduction. Catecholamines are released into the circulation of fishes in response to hypoxia and it was hypothesized that adrenergic stimulation of O₂ receptors might contribute to the observed reflex responses. Epinephrine and norepinephrine stimulate O₂ receptors and ventilation in mammals (Fidone and Gonzalez, 1986). Although fish respond to large dosages of epinephrine and norepinephrine (100-1000 nmol/kg) with hyperventilation (lower dosages, 5 nmol/kg, have little or no effect in intact fish), the afferent neural activity from the branchial O₂ receptors was not affected by these neurochemicals. Thus, ventilatory responses to increased circulating catecholamines do not appear to be mediated by branchial O₂ receptors. Inhibition of O₂ receptor activity by propranolol was probably due to indirect effects. Dopamine elicited a dose-dependent brief burst of chemoreceptor activity followed by inhibition but had only modest effects on DA blood pressure and inhibited opercular pressure amplitude in intact fish. Serotonin (5-Hydroxytryptamine) caused a transient increase in chemoreceptor activity. In intact fish, serotonin, stimulated heart rate, decreased DA blood pressure and stimulated ventilation. Cholinergic agonists (acetylcholine, nicotine and muscarine) significantly stimulated O₂ receptor discharge. Acetylcholine and nicotine increased heart rate, DA blood pressure and ventilation in intact fish, whereas, muscarine decreased heart rate and DA blood pressure and increased ventilation. Atropine inhibited O₂ receptor activity but had little affect on ventilation in intact fish. Cholinergic mechanisms appear to be more important than adrenergic mechanisms in controlling the cardiovascular and ventilatory reflex responses mediated by branchial Gysensitive chemoreceptors. The response characteristics of branchial O₂-sensitive chemoreceptors indicates that they are homologous to the O₂ receptors of the mammalian aortic and carotid bodies.

Text

2011-01-28

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http://hdl.handle.net/2429/30963

Zoology

University of British Columbia

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