Abstract

The effects of ambient O2 partial pressure and CO2 partial pressure on the intensity of rainbow trout (Oncorhynchus mykiss) red blood cell β-adrenergic Na+/H+ exchange were investigated. This was accomplished in vitro by continuously monitoring whole blood extracellular pH, partial pressures of O2 and CO2 and by measuring red blood cell water content and Na+ concentration before and 30 min after the addition of a catecholamine mixture (final nominal concentrations: 250 nmol·l-1 adrenaline and 20 nmol·l-1 noradrenaline). The experiments were performed under six different initial conditions combining two ambient partial pressures of CO2 (1.50 and 6.75 torr) and three ambient partial pressures of O2 (15, 30 and 150 torr). The activation of red blood cell Na+/H+ exchange (as indicated by marked reductions of whole blood pH) was followed by transient reductions in blood partial pressures of CO2 and O2 (2 min) resulting from the shift of the CO2/HCO3 - equilibrium within the cell and the subsequent binding of O2 to the haemoglobin. The initial reduction in blood CO2 partial pressure was followed by a rise reflecting the titration of plasma HCO3 - by extruded H+. At low partial pressure of CO2 (1.50 torr) there was a pronounced stimulatory effect of hypoxia on the initial intensity of the extracellular acidification (5 min), whereas at high CO2 partial pressure (6.75 torr) hypoxia actually lowered the extent of the initial acidification. In all cases, Na+/H+ exchange activation was accompanied by increases in cell water content and red blood cell Na+ levles when measured 30 min after addition of catecholamines. Both hypercapnia and hypoxia increased the magnitude of these changes although the largest changes in cell water content and Na+ levels were observed under hypercapnic conditions. Thus, the long-term activity (as determined by measuring cell water and Na+ levels) of the Na+/H+ exchanger was enhanced both by hypercapnia and hypoxia regardless of the initial CO2 partial pressure. The initial activity (5 min), on the other hand, although stimulated by hypercapnia was influenced by hypoxia in opposing directions depending upon the initial CO2 partial pressure of the blood.

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