Reciprocal modulation of O2 and CO2 cardiorespiratory chemoreflexes in the tambaqui

Abstract

This study examined the effect of acute hypoxic and hypercapnic cardiorespiratory stimuli, superimposed on existing cardiorespiratory disturbances in tambaqui. In their natural habitat, these fish often encounter periods of hypoxic hypercapnia that can be acutely exacerbated by water turnover. Tambaqui were exposed to periods of normoxia, hypoxia, hyperoxia and hypercapnia during which, externally oriented O 2 and CO 2 chemoreceptors were further stimulated, by administration into the inspired water of sodium cyanide and CO 2 -equilibrated water, respectively. Hyperoxic water increased the sensitivity of the NaCN-evoked increase in breathing frequency (f R ) and decrease in heart rate. Hypoxia and hypercapnia attenuated the increase in f R but, aside from blood pressure, did not influence the magnitude of NaCN-evoked cardiovascular changes. Water PO 2 influenced the magnitude of the CO 2 -evoked cardiorespiratory changes and the sensitivity of CO 2 -evoked changes in heart rate and blood flow. The results indicate that existing respiratory disturbances modulate cardiorespiratory responses to further respiratory challenges reflecting both changes in chemosensitivity and the capacity for further change.

Zebrafish (Danio rerio) gill neuroepithelial cells are sensitive chemoreceptors for environmental CO2

“…There is also some evidence that the primary CO 2 /pH sensor is independent of the O 2 sensor in some cases; the effects of CO 2 and/or pH are not mediated through changes in the affinity of an O 2 sensor in carotid body glomus cells (Dasso et al 2000). However, there are also data suggesting that CO 2 chemosensitivity may be modulated by hypoxia (Reid et al 2005; see review by Lahiri & Forster, 2003). It is interesting that while the glomus cells of the carotid body proliferate in response to chronic hypoxia, the density of the analogous population of gill NECs (those possessing 5‐HT) in zebrafish is unaffected by long‐term hypoxia (Jonz et al 2004; Vulesevic et al 2006).…”

Fish and hyperoxia—From cardiorespiratory and biochemical adjustments to aquaculture and ecophysiology implications

“…The cross symbol represents the mean O 2 level of normoxic treatments in all studies (96.2% air saturation). Numbers indicate references as follows: 1 (McArley et al., 2018), 2 (Wilkes et al., 1981), 3 (Reid et al., 2005), 4 (Takeda, 1990), 5 (Soncini & Glass, 2000), 6 (Randall & Jones, 1973), 7 (Wood & Jackson, 1980) 8 (Thomas et al., 1983), 9 (Kinkead & Perry, 1990), 10 (Mark et al., 2002), 11 (Heisler et al., 1988), 12 (Forgue et al., 1989), 13 (Le Moigne et al., 1986)…”

Control of air-breathing in fishes: Central and peripheral receptors

“…The primary sites of peripheral O 2 sensing in fish appear to be the gills (including the pseudobranch in those species that possesses one) and orobranchial cavity (Laurent and Rouzeau, 1972;Randall and Jones, 1973;Butler et al, 1977;Daxboeck and Holeton, 1978;Smith and Davie, 1984;Smatresk et al, 1986;Burleson and Smatresk, 1990;McKenzie et al, 1991a;Burleson and Milsom, 1993;Sundin et al, 1999Sundin et al, , 2000Milsom et al, 2002). Chemoreceptors in the orobranchial cavity are innervated by branches of the Vth (trigeminal) and/or VIIth (facial) cranial nerves, those on the pseudobranch by branches of the VIIth and/ or IXth (glossopharyngeal) cranial nerves, and those on the gill arches by branches of the IXth and/or Xth (vagus) cranial nerves (Butler et al, 1977;Burleson et al, 1992;Milsom et al, 2002;Reid et al, 2005). Some of these chemoreceptors respond only, or preferentially, to changes in external (water) O 2 , others respond only, or preferentially, to changes in internal (blood) O 2 , and some respond to both (Milsom and Brill, 1986;Burleson and Milsom, 1993).…”

“…Thus, the hypoxic stimulation of the gill NECs seems to initiate the adaptive cardiorespiratory reflexes, which allows for O 2 uptake and delivery to meet metabolic demands (Zachar and Jonz, 2012). Different responses can be triggered by distinct types of NECs, and it is not yet clear whether interspecific differences in the location of the NECs or in the responses triggered by each type of NECs might be attributable to differences in lifestyle (active versus sluggish fish), habitat (hypoxia tolerant versus intolerant fish) or phylogeny (Milsom et al, 1999;Perry and Gilmour, 2002;Reid et al, 2005;Coolidge et al, 2008).…”