The conversion of plasma HCO 3 (-) to CO 2 by rainbow trout red blood cells in vitro: adrenergic inhibition and the influence of oxygenation status.

This study employed a recently developed radioisotopic assay (Wood and Perry 1991) to examine the inhibition, induced by catecholamines, of the conversion of plasma HCO 3 (-) to CO2 in acidotic trout blood, and the influence of oxygenation status on the response. Blood was incubated in vitro at PCO 2= 2 torr, and 10(-6) M noradrenaline was employed as the adrenergic stimulus. In particular we investigated whether the inhibition of plasma HCO 3 (-) conversion could be explained by a limited supply of H(+)s for the intracellular HCO 3 (-) dehydration reaction because of competition by the adrenergically activated Na /H(+) exchanger. Hypoxia (PO 2= 15 torr) was employed as a tool to intensify this competition. Hypoxia raised RBC pHi, pHe, and plasma total CO2 concentration (CCO 2) by the Haldane effect, and increased the magnitude of Na(+)/H(+) activation, expressed as the change in the transmembrane pH gradient (pHe-pHi). However hypoxia did not alter the inhibition of the conversion of plasma HCO 3 (-) to CO2 caused by noradrenaline. Hypoxia itself stimulated the RBC-mediated conversion of plasma HCO 3 (-) to CO2 by about 20% in the presence or absence of noradrenaline. The conversion rate was strongly correlated with pHe, pHe-pHi, and plasma CCO 2 in these experiments, but not with pHi. We conclude that adrenergically mediated inhibition in the conversion of plasma HCO 3 (-) to CO2 by trout RBCs is not due to competitive limitation on intracellular H(+)s, but rather to changes in the electrochemical gradient for HCO 3 (-) entry and/or to CO2 recycling from plasma to RBC. The deoxygenated condition helps to promote CO2 excretion at the level of the RBC.