Toxolasma texasensis acclimated to an artificial pondwater (PW) maintained a concentration of SO4 in the blood of about 1-2 mmol l(-1) . The anion transport inhibitor DIDS (5,5'-diisothiocyanatostilbene 2, 2'-disulfonic acid) reduced the uptake of 35SO4 from the bathing medium by 54%. The clearance of polyethylene glycol (PEG) injected into the blood of T. texasensis ranged between 0.8 and 1.3 ml g(-1) dry tissue h(-1), and provided an estimate of renal filtration in PW-acclimated animals. The clearance of radioactive 35SO4 simultaneously injected into the same animal was about 16% of the PEG clearance, suggesting that sulfate was being reabsorbed by the kidney. Para-aminohippuric acid was cleared about 4.6 times faster than PEG, indicating that this organic acid was subjected to secretion in addition to filtration. When the normal osmotic gradient was abolished by acclimating T. texasensis to 10% seawater (SW), the PEG clearance decreased to 0.17 ml g(-1) dry tissue h(-1). Sulfate clearance in animals acclimated to PW or 10% SW was the same. However, in mussels acclimated to 10% SW, the calculated amount of SO4 reabsorbed was significantly reduced relative to mussels acclimated to PW. T. texasensis conserved SO4 when acclimated to PW, and reduced reabsorption when acclimated to the sulfate-rich 10% SW. When mussels acclimated to 10% SW were returned to PW, there was a transient increase in sulfate clearance during the first 8 h because filtration exceeded reabsorption.

The influx of Cl- across isolated frog skin bathed on the outside by 0.8 mM NaCl is about 100 nmol cm-2 h-1, which is approximately twice the Cl- influx in intact animals. The influx consists of diffusion (1%), exchange diffusion (38%), and active transport (60%). About 80% of the influx is independent of Na+ in the outer bath and is also independent of concomitant inward movement of cations. Chloride is exchanged for anions, probably HCO-3. The Cl- transport system is saturable; Vmax is about 200 nmol cm-2 h-1, and Ks is about 0.7 mM Cl-. High external concentrations of NaCl increase unidirectional fluxes of Cl- and urea, indicating a change in paracellular pathways. Active transport of Cl- is temperature sensitive (Q10 equals 2.68) and is inhibited by cyanide, dinitrophenol, iodoacetic acid, iodide, thiocyanate, and acetazolamide. The Na-independent component of JClin was unaffected by amiloride, ouabain, or eserine, all of which inhibit Na+ transport.

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