The modes of ammonia transport across the gill epithelium of the dogfish pup (Squalus acanthias) were investigated using an isolated, perfused head preparation. During perfusion for 2–3 h there was no obvious oedema of gill lamellae, the head was haemodynamically responsive to near-in-vivo concentrations of adrenaline, and the transepithelial potential was +1.9mV (perfusate relative to irrigate) and was unaffected by any of the potential inhibitors used in these tudies. The rate of ammonia efflux was somewhat above in vivo levels, was not due to structural leaks (which averaged less than 1%), declined by 17 % during a second, 20-min efflux period, but was stable during a third efflux period. Addition of bumetanide to the perfusate inhibited ammonia efflux by 17 % compared with the control, but subsequent addition of ouabain had no effect. Amiloride added to the irrigate in the presence of ouabain in the perfusate had no effect on ammonia efflux. Ammonia efflux was stimulated by specific increases in perfusate PNH3 much more (1100 times) than by specific increases in perfusate NH4+ concentrations. Given a pK of ammonia of 9.75, we calculate that 6% of the total ammonia efflux is via ionic diffusion of NH4+, 77% via non-ionic diffusion of NH3, and 17 % via a bumetanide-sensitive Na++NH4++2Cl cotransport system. Basolateral or apical Na+/NH4+ exchange apparently is not involved in ammonia transport across this epithelium.

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