Control and consequences of adrenergic activation of red blood cell Na+/H+ exchange on blood oxygen and carbon dioxide transport in fish

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Abstract
The catecholamines, adrenaline and noradrenaline, are released into the circulation of fish during a variety of physical and environmental disturbances that share the common feature of a requirement for enhanced blood oxygen transport. Indeed, the dominant factor controlling the mobilization of catecholamines from chromaffin tissue is a depression of blood oxygen content usually coinciding with a reduction of hemoglobin‐O2 (Hb‐O2) binding to 50–60% saturation. The elevation of plasma catecholamine levels, under such conditions, activates a β‐adrenergic cyclic AMP‐dependent Na + /H+ exchanger on the red blood cell (rbc) membrane. The adrenergic responsiveness of the rbc Na + /H+ exchanger to catecholamines varies both within and between species. Such inter‐ and intra‐specific differences may reflect, in part, the availability of cell surface β‐adrenoceptors that are functionally coupled to adenylate cyclase. The activation of rbc Na + /H + exchange and the accompanying profound adjustments of intracellular and extracellular acid‐base status, nucleoside triphosphate (NTP) levels, and cooperativity of Hb‐O2 binding have important consequences on both O2 and CO2 transfer and transport in the blood that vary markedly at the sites of oxygenation (the gill) and deoxygenation (the tissues) thereby enabling simultaneous amelioration of O2 loading and unloading. At the gill, oxygen transfer is enhanced owing to increases in Hb‐O2 affinity and capacity while at the tissues, oxygen delivery is facilitated by a reduction of Hb‐O2 affinity. This reduction in affinity at the tissues is a consequence of the combined effects of increased cooperativity of Hb‐O2 binding and a rise in venous PCO2 (PvCO2) caused by the titration of HCO3− by H+ extruded by the rbc Na + /H+ exchanger. This elevation of PvCO2 may contribute to the rise in arterial PCO2 (PaCO2) observed after adrenergic activation of rbc Na + /H+ exchange that is caused primarily by impairment of rbc CO2 excretion related to modification of the intracellular acid‐base status.

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