Socially subordinate rainbow trout (Oncorhynchus mykiss) experience chronic stress that impacts upon a variety of physiological functions, including Na(+) regulation. Owing to the tight coupling between Na(+) and Cl(-) uptake and, respectively, H(+) and HCO(3)(-) loss at the gill, ionoregulatory changes associated with social status may affect
acid-base regulation. The present study assessed the responses of dominant, subordinate and control trout to
hypercapnia (1% CO(2)) to test this hypothesis. Social status appeared to impact net
acid excretion (J(net)H(+)) as subordinate individuals failed to increase net
acid flux in response to
hypercapnia. However, blood
acid-base status was found to be unaffected by social status before or during hypercapnic exposure, indicating that subordinate fish were as effective as dominant or control trout in achieving compensation for the
acid-base disturbance induced by hypercapnic exposure. Compensation in all groups involved decreasing Cl(-) uptake in response to
hypercapnia. The branchial activities of both Na(+),K(+)-
ATPase (NKA) and V-type
H(+)-ATPase were affected by social interactions and/or exposure to
hypercapnia. Branchial NKA activity was higher but V-
ATPase activity was lower in control fish than in dominant or subordinate trout. In addition, control and subordinate but not dominant trout exposed to 24h of
hypercapnia exhibited significantly higher branchial V-
ATPase activity than fish maintained in normocapnia. Collectively, the data suggest that subordinate trout are able to regulate blood pH during a
respiratory acidosis.