Prolactin is probably implicated in the control of physiological adaptation to sublethal acid stress in tilapia. Exposure of fish to water at pH 3 caused death within 72 hr, which was associated with pronounced hemodilution. At pH 4 mortality was low, although a substantial and rapid decrease in plasma osmolality, plasma Na+, and plasma total Ca was observed. These effects were at least partly due to increased permeability of the gills for water and ions. After a few days at pH 4, restoration of plasma osmolality, Na+, and total Ca was noticeable. Control levels were reached after 5 days for Ca, and after 10 days for osmolality, Na+, and branchial osmotic water permeability. Prolactin secretion increased markedly during acid exposure, as was established by morphometrical and biochemical methods. In tilapia, administration of prolactin is known to raise plasma osmolality, Na+, and plasma total Ca. This hormone further has been shown to reduce branchial osmotic water permeability. It is concluded therefore that the restoration of plasma electrolytes and branchial osmotic water permeability during chronic acid stress are causally connected with the observed stimulation of prolactin secretion.