β-adrenergic signal transduction in fish: interactive effects of catecholamines and cortisol

Abstract

The elevation of plasma catecholamine levels during acute stress initiates a series of compensatory physiological and biochemical mechanisms to alleviate the disruptive effects of stress on blood oxygen transport. Of particular importance is the β-adrenergic activation of a Na(+)/H(+) antiporter associated with the red blood cell (rbc) membrane. Upon activation, the Na(+)/H(+) antiporter extrudes H(+) from the rbc and the resultant alkalinization of the rbc interior serves to enhance both the affinity and the capacity of haemoglobin O2 binding. The activation of the Na(+)/H(+) exchanger is dependent upon the intracellular accumulation of cyclic AMP. The extent of cyclic AMP accumulation is determined, in part, by the number and/or affinities of cell surface β-adrenoreceptors. Recent studies have shown that the number of cell surface β-adrenoreceptors are rapidly increased during acute hypoxia and that this phenomenon may explain the enhanced responsiveness of hypoxic rbc's to exogenous catecholamines.In certain instances, plasma catecholamine and cortisol levels rise concurrently. We recently have shown that chronic (10 day) elevation of cortisol levels, in vivo, or short-term (24h) elevation, in vitro, caused significant elevation of internalized β-adrenoreceptors. Upon exposure of the rbc's to hypoxia, these additional receptors are rapidly recruited to the cell surface where they become functionally coupled to adenylate cyclase. Ultimately, therefore, chronic elevation of plasma cortisol levels increases the responsiveness of the rbc to circulating catecholamines. We recently have identified similar enhancement of cell surface β-adrenoreceptors by cortisol and increased physiological responsiveness (glycogenolysis) to catecholamines in trout hepatocytes.Thus, chronic elevation of cortisol levels appears to be generally adaptive for increasing the sensitivity of the β-adrenergic signal transduction system of at least two cell types (rbc's, hepatocytes) involved in the amelioration of acute stress when plasma catecholamine levels rise.

A putative β2‐adrenoceptor from the rainbow trout (Oncorhynuchus mykiss)

“…Trout red blood cell β‐ARs control the activity of a Na/H + exchanger (βNHE) located in the red cell plasma membrane. Stimulation of red blood cell β‐ARs leads to βNHE activation that ultimately results in an increased hemoglobin/oxygen binding affinity during times of stress [18]. Our results do not concur with previous pharmacological studies [39], suggesting that a β 2 ‐AR subtype controls the activity of the trout red blood cell βNHE.…”

“…In addition, fish β‐ARs elicit responses unique to particular species or groups of fish. For example, catecholamine release causes an increase in hemoglobin/oxygen binding affinity in the rainbow trout erythrocyte by activation of a red blood cell β‐AR [18].…”

LOW WATER TEMPERATURE AND ITS EFFECTS ON STRESS RESPONSE OF GREY MULLETS Mugil cephalus ACCLIMATED IN FRESHWATER

“…The hypothalamus-pituitary-interrenal activity was triggered by stressor, which resulting in cortisol secretion (Perry & Reid, 1993) and increased the blood glucose (Tomasso et al, 1980). In this study, low water temperature as a stressor tend to increase the stress of grey mullets.…”

The effects of hypoxia, in vivo, on red blood cell ?-adrenoceptors in the rainbow trout, Oncorhynchus mykiss

“…Furthermore, when blood from cortisol-treated fish was exposed to hypoxia in vitro, an increase in the number of 0B-adrenoceptors on the rbc surface occurred, presumably, as receptors were mobilized from the internal pool. Additionally, the results of several previous studies (Martilla and Nikinmaa 1988;Reid et al 1993) have demonstrated an increase in the number of cell surface receptors in response to hypoxia, in vitro, in the absence of elevated cortisol levels (see review by Perry and Reid 1993). A similar hypoxia protocol using uncannulated fish demonstrated that plasma cortisol levels (ranging between 15-50 ng ml-') were not different, compared with normoxic fish, during 48h of hypoxia at a PwO 2 of 8.0 kPa (unpublished observations).…”