SUMMARY1. Hypotonic stress unmasked inward and outward K+ and Cl-movements in rat thymocytes. This KCl flux stimulation was reduced by DIOA (dihydroindenyl-oxyalkanoic acid), but not by DIDS (4,4'-diisothiocyanostilbene-2,2'-disulphonate), quinidine, DPAC 144 (5-nitro-2-(2-phenylethyl-amino)-benzoic acid), bumetanide or ouabain.2. In isotonic media (308 + 5 mosmol kg-'), the cells exhibited the following DIOA-(ii) a Cl-efflux of 68 + 21 mmol (I cells. h)-1 (n = 3), (iii) a Rb+ influx of 9-7 + 3 9 mmol (1 cells.h)-1 (n = 6) and (iv) a Cl-influx of 94+4-1 mmol (1 cells.h)-1 (n = 6). 4. The DIOA-sensitive membrane carrier catalysed net outward KCl extrusion (the outward/inward flux ratio was 5-7 in isotonic media and 20 in hypotonic media at 189 mosmol kg-'). Inhibition of DIOA-sensitive 36C1-efflux by cell K+ depletion suggested coupling of outward K+ and Cl-fluxes. Conversely, inward K+ and Clfluxes were found to be uncoupled in NO3-media and in K+-free media.5. The results clearly show that rat thymocyte membranes possess a 1: 1 K+-Clco-transport system which is strongly activated by hypotonic shock and catalyses net KCl extrusion.

SUMMARY1. DIOA (dihydroindenyl-oxy-alkanoic acid), a potent inhibitor of the K+-Cl-cotransport system, fully blocked regulatory volume decrease (RVD) in swelled rat thymocytes, with an IC50 of 2-2 + 0 5 x 10-5 mol 1-1 (mean + S.D., n = 4). Conversely, RVD was resistant to quinine, quinidine, apamin, cetiedil, amiloride, bumetanide and DIDS (4,4'-diisothiocyanostilbene-2,2'-disulphonate).2. DIOA-sensitive RVD followed mono-exponential kinetics, with th (half-lifetime) of 1-3 min and maximal capacity (Cmax) of about 55 % of the initial cell swelling.Cmax and the initial rate of RVD (V.) were both linear functions of the increase in cell volume.3. RVD was: (i) slightly increased by replacing external Cl-by NO3-, (ii) reversed by replacing external Na+ by K+ (in the presence of external Cl-) and (iii) inhibited by cell K+ depletion. All these phenomena were blocked by DIOA (86 jmol 1-1).4. Increased membrane potassium permeability by valinomycin was unable to accelerate RVD or RVD reversal.5. In the presence of DIOA, thymocytes responded like osmometers (the relative cell volume was a linear function of the reciprocal of the relative osmolality) in a large range of osmolalities.6. The results strongly suggest that RVD in rat thymocytes is mediated by the K+-Cl-co-transport system.

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Chronic clofibrate treatment suppressed the hemodynamic manifestations and increased temperature of hyperthyroidism, an effect that can be produced by direct antithyroid effects. However, clofibrate administration did not modify the morphologic, metabolic, or renal alterations of hyperthyroid rats, indicating specificity in the antithyroid actions of clofibrate.