We adapted killifish to defined freshwater (FW: 1.0 mM Na+, 1.0 mM Cl−, + 0.1 mM Ca2+) and by fluorescence light microscopy and scanning and transmission electron microscopy found that the opercular epithelium retained mitochondria rich (MR) cells that were significantly larger but less numerous than in SW‐acclimated tissues. Opercular epithelia mounted in vitro with FW bathing the mucosal surface take up Cl− against a large negative inside transepithelial potential (Vt, grand mean −64.1 mV) and concentration gradient; the observed flux ratio was significantly different (P < 0.001) from that predicted for passive ion distribution but the net flux was consistently negative. The Na+ flux ratio suggested that Na+ was passively distributed. Vt was largely a Na+ diffusion potential, based on unilateral manipulations of [Na+]. Cl− unidirectional uptake was unaffected by mucosally added SITS (0.1 mM) but was inhibited by SCN− (1.0 mM) and by anaerobiosis. Killifish transferred from SW to FW for 48 h had reduced Cl− secretion by the opercular epithelium compared to SW controls but had not yet developed Cl− uptake, indicating a slow adaptive process for development of Cl− absorptive transport. Opercular epithelia of FW adapted fish, if bathed with isotonic saline on both sides, has a modest net Na+ and Cl− uptake, unlike SW opercular epithelium that strongly secretes Cl− under similar conditions. FW killifish opercular epithelium may provide a model to study ion regulation by euryhaline fish. J. Exp. Zool. 277:23–37, 1997. © 1997 Wiley‐Liss, Inc.

To examine the role of cortisol in seawater osmoregulation in a euryhaline teleost, adult killifish were acclimated to brackish water (10 per thousand) and RU486 or vehicle was administered orally in peanut oil daily for five days at low (40 mg.kg(-1)) or high dose (200 mg.kg(-1)). Fish were transferred to 1.5 x seawater (45 per thousand) or to brackish water (control) and sampled at 24 h and 48 h after transfer, when Cl- secretion is upregulated. At 24 h, opercular membrane Cl- secretion rate, as Isc, was increased only in the high dose RU486 group. Stimulation of membranes by 3-isobutyl-1-methylxanthine and cAMP increased Isc in vehicle treated controls but those from RU486-treated animals were unchanged and membranes from brackish water animals showed a decrease in Isc. At 48 h, Isc increased and transepithelial resistance decreased in vehicle and RU486 groups, compared to brackish water controls. Plasma cortisol increased in all groups transferred to high salinity, compared to brackish water controls. RU486 treated animals had higher cortisol levels compared to vehicle controls. Vehicle treated controls had lower cortisol levels than untreated or RU486 treated animals, higher stimulation of Isc, and lower hematocrit at 24 h, beneficial effects attributed to increased caloric intake from the peanut oil vehicle. Chloride cell density was significantly increased in the high dose RU486 group at 48 hours, yet Isc was unchanged, suggesting a decrease in Cl- secretion per cell. Thus cortisol enhances NaCl secretion capacity in chloride cells, likely via glucocorticoid type receptors.

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Brook trout (Salvelinus fontinalis) urinary bladder in vitro had a low serosa-positive transepithelial potential (6.7 +/- 1.2 mV), low transmural conductance (0.23 +/- 0.03 mS. cm-2), and net absorptive transport of Na+ and Cl-. The net flux of Na+ was equivalent to that of Cl- and much larger than the membrane current, indicating neutral NaCl uptake. Na+ uptake was not coupled to that of Cl-, since absorptive Na+ transport continued in (Cl-)-free media. In the absence of Cl-, the net absorption of Na+ was accompanied by net secretion of titratable acidity, suggestive of Na+-H+ exchange on the luminal surface. Active Cl- transport persisted in dilute (2.0 mM) tetraethylammonium chloride with zero K+ and zero Na+, indicating full independence of the Cl- transport from cation coupling and suggesting the presence of Cl(-)-HCO-3 exchange. The kinetics of Cl- uptake (K1/2 = 35-37 mM, maximal transport rate = 3.0-3.4 mu eq . cm-2 . h-1) were not significantly affected by removal of mucosal Na+ . Cl- uptake was inhibited partially by 10(-4) M amiloride but not by 10(-4) M bumetanide. The results strongly support a model for active NaCl transport involving paired ion exchangers, likely located at the luminal membrane.