The Ionoregulatory Responses to Hypoxia in the Freshwater Rainbow Trout Oncorhynchus mykiss

We utilized the rainbow trout, a hypoxia-intolerant freshwater teleost, to examine ionoregulatory changes at the gills during hypoxia. Progressive mild hypoxia led first to a significant elevation (by 21%) in J(influx)(Na) (measured with Na-22), but at 4-h hypoxia when Po-2 reached similar to 110 mmHg, there was a 79% depression in J(influx)(Na). Influx remained depressed during the first hour of normoxic recovery but was restored back to control rates thereafter; there were no significant changes in J(efflux)(Na) or J(net)(Na). A more prolonged (8 h) and severe hypoxic (similar to 80 mmHg) exposure induced a triphasic response whereby J(influx)(Na) was significantly elevated during the first hour, as during mild hypoxia, but returned to control rates during the subsequent 3 h. Thereafter, rates started to gradually increase and remained significantly elevated by about 38% through to 8 h of hypoxia. A similar triphasic trend was observed with J(efflux)(Na) but with larger changes than in J(influx)(Na), such that negative Na+ balance occurred during the hypoxic exposure. Net K+ loss rates to the water approximately doubled. There were no significant alterations in ammonia excretion rates in either of the hypoxia regimes. Branchial Na+/K+-ATPase activity did not change during 4 h at Po-2 similar to 80 mmHg or return to normoxia; H+-ATPase activity also did not change during hypoxia but was significantly depressed by similar to 75% after 6 h of normoxic recovery. Scanning electron microscopy revealed that within 1 h of exposure to Po-2 similar to 80 mmHg, exposed mitochondria-rich cell (MRC) numbers increased by 30%, while individual MRC exposed surface area and total MRC surface area both increased by three-to fourfold. MRC numbers had decreased below control levels by 4 h of hypoxia, but surface exposure remained elevated by approximately twofold, a response that persisted through 6 h of normoxic recovery. Environmental hypoxia induces complex changes in gill ionoregulatory function in this hypoxia-intolerant species that are very different from those recently reported in the hypoxia-tolerant Amazonian oscar.