Abstract This study evaluated the physiological effects of waterborne silver (added as AgNO 3) on seawater fish, using acute (48–72 h) high level exposures (250–650 μg/l Ag) on tidepool sculpins ( Oligocottus maculosus), and chronic (up to 21 day) low level exposures (1.5–50 μg/l Ag) on tidepool sculpins, plainfin midshipmen ( Porichthys notatus), and rainbow trout ( Oncorhynchus mykiss). Sculpins were tested at different salinities. Acclimation to lower salinity (18 vs 30 ppt) led to altered physiology, with higher ammonia excretion ( J Amm), lower oxygen consumption M O 2 , and lower branchial and intestinal Na +/K +-ATPase activities, but no difference in drinking rate. Short-term exposure to high silver levels tended to stimulate M O 2 , J Amm, and drinking rate. However, long-term exposure to low levels of silver depressed both J Amm and M O 2 , and also led to decreased drinking rates. Both inhibition and stimulation of Na +/K +-ATPase activity occurred, dependent upon length and concentration of exposure, salinity (18 vs 30 ppt), tissue (gill vs intestine), and fish species (sculpin vs midshipmen vs rainbow trout). While the effects were variable, due to differing balances between inhibitory and compensatory responses, chronic silver exposure significantly altered Na +/K +-ATPase activity levels in almost all tests. In total, these findings reinforce the view that intestinal osmoregulatory function (drinking, Na +/K +-ATPase activity) is an important site of toxic impact for waterborne silver, that gill Na +/K +-ATPase activity is also a site of impact, and that chronic exposures at silver concentrations (1.5, 14.5 μg/l Ag) close to current or proposed water quality guidelines (albeit much higher than normal environmental levels), exert a variety of sublethal effects on marine teleosts.