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(Na)(influx) (measured with 22Na), but at 4-h hypoxia when PCO2 reached approximately 110 mmHg, there was a 79% depression in J(Na)(influx). 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(Na)(efflux) or J(Na)(net). A more prolonged (8 h) and severe hypoxic (approximately 80 mmHg) exposure induced a triphasic response whereby J(Na)(influx) 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(Na)(efflux) but with larger changes than in J(Na)(influx), 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 PO2 approximately 80 mmHg or return to normoxia; H+-ATPase activity also did not change during hypoxia but was significantly depressed by approximately 75% after 6 h of normoxic recovery. Scanning electron microscopy revealed that within 1 h of exposure to PO2 approximately 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.
Iftikar
Fathima I
FI
Department of Biology, McMaster University, Hamilton, Ontario L8S4K1, Canada. iftikafi@gmail.com
Matey
Victoria
V
Wood
Chris M
CM
D000222:Adaptation, Physiological / Q000502:physiology; D000641:Ammonia / Q000378:metabolism; D000818:Animals; D005880:Gills / Q000033:anatomy & histology / Q000378:metabolism / Q000502:physiology; D000860:Hypoxia / Q000503:physiopathology*; D008855:Microscopy, Electron, Scanning; D008928:Mitochondria / Q000378:metabolism / Q000648:ultrastructure; D017686:Oncorhynchus mykiss / Q000502:physiology*; D012964:Sodium / Q000378:metabolism / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism / Q000502:physiology
D000641:Ammonia; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase