DIFFERENT MECHANISMS OF ACID-BASE REGULATION IN RAINBOW-TROUT (ONCORHYNCHUS-MYKISS) AND AMERICAN EEL (ANGUILLA-ROSTRATA) DURING NAHCO3 INFUSION

Rainbow trout (Oncorhynchus mykiss) and American eels (Anguilla rostrata) were infused intra-arterially with NaHCO3 (similar to 800 mu mol/kg/b) to assess their acid-base regulatory mechanisms during metabolic alkalosis. In both species, plasma PH and [HCO3-] increased during infusion, although the changes were more pronounced in the eel. In trout, pH and [HCO3-] were returned to preinfusion values by 12 h after infusion was stopped while in the eel there was only incomplete clearance of accumulated [HCO3-] during the 24-h postinfusion period. In each case, approximately 20 mmol/L of HCO3- was removed from the plasma during postinfusion. The predominant mechanism employed by both trout and eel to regulate blood acid-base status during alkalosis was manipulation of branchial net Cl- flux (J(net)(Cl-)), although this was accomplished with markedly different strategies. Trout relied primarily on adjustments of branchial Cl- uptake (J(in)(Cl-)) to control J(net)(Cl-). In the eel, however, owing to the absence of an appreciable influx component to J(net)(Cl-), regulation of Cl- efflux was the dominant strategy. The surface area of gill filament chloride cells (CCs) was increased during alkalosis in trout and appeared to be the mechanism underlying the stimulation of J(in)(Cl-) and clearance of the infused base load. In the eel, CC surface area was low, and not significantly altered by NaHCO, infusion. In summary, different strategies were used by trout and eel to regulate blood acid-base status during NaHCO, infusion. Trout relied on (i) elevation of J(in)(Cl-) (ii) reduction of J(out)(Cl-), and (iii) intracellular buffering. In contrast, the eel relied almost exclusively on reduction of J(out)(Cl-). Manipulation of CC surface area to increase J(in)(Cl-) or the use of intracellular buffering appeared to be unimportant for regulating metabolic alkalosis in eel.