The Effects and Physiological Consequences of Raised Levels of Cortisol on Rainbow Trout (Oncorhynchus Mykiss) Erythrocyte β-Adrenoreceptors

We have investigated the influence of cortisol on the β-adrenoreceptor population of rainbow trout [Oncorhynchus mykiss (Walbaum)] erythrocytes and determined what impact it has on the adrenergic responsiveness of erythrocytes in vitro to exogenous catecholamines. To do so, the erythrocyte β-adrenoreceptors were characterized in fish with chronically elevated plasma cortisol levels (118±5.9ngml⁻¹, >10 days) and compared with shams, using radioreceptor assay techniques. The number of ‘internalized’, low-affinity receptors was increased when cortisol levels were raised, but the number of high-affinity, ‘surface’ receptors was not altered. The physiological significance of this response was ascertained by assessing the in vitro sensitivity (or responsiveness) of erythrocytes to adrenaline and noradrenaline (10–1000 nmol I⁻¹) under normoxic or hypoxic conditions. Erythrocyte sensitivity to catecholamines, as determined by changes in both whole-blood pH (ΔpHe) and intracellular cyclic AMP content, was greater in hypoxic than in normoxic blood. Although cortisol further enhanced the responsiveness of erythrocytes to catecholamines, this amplification in sensitivity was observed only during hypoxia.

When the radioreceptor assay was conducted using erythrocytes from the catecholamine sensitivity experiments, results were consistent with initial receptor density data. An increase in surface receptor density was associated with hypoxia in vitro. This hypoxia-specific increase in surface β-adrenoreceptors was significantly enhanced in the cortisol-treated erythrocytes, showing that cortisol had a significant impact on erythrocyte β-adrenoreceptor dynamics in addition to the direct influence of hypoxia.

This study has shown (1) that, by itself, in vitro hypoxia simultaneously initiates the movement of internal receptors to the cell surface, where they become physiologically active, and the replenishment of the internal receptor pool,(2) that cortisol increases receptor availability by increasing the internal pool of low-affinity receptors in the absence of any stimulus for receptor mobilization, and (3) that the sensitivity of erythrocytes to catecholamines is directly proportional to the number of high-affinity receptors present at the erythrocyte surface. Thus, we suggest that, under conditions of chronic stress, cortisol may pre-adapt the erythrocytes to receive additional physiological inputs that can ultimately enhance respiratory performance beyond that which would be possible in the absence of chronically elevated levels of cortisol.