Seasonality of the red blood cell stress response in rainbow trout (Oncorhynchus mykiss)

The beta-adrenergic stress response in red blood cells (RBCs) of rainbow trout shows seasonal changes in expression. We have explored the mechanisms underpinning this response by following, over a period of 27 months, changes in P-adrenergic receptor (beta-AR) binding characteristics, beta-adrenergically stimulated RBC Na+/H+ exchanger (betaNHE) activity, together with beta-AR and betaNHE mRNA levels and plasma steroid hormone and lactate levels. These parameters were measured at approximately monthly intervals in a single population of fish held under semi-natural conditions. Membrane-bound, high-affinity beta-ARs were present in RBCs at all sampling times, varying from 668 +/- 112 receptors cell(-1) to 2654 +/- 882 receptors cell(-1) (mean +/- S.E.M.; N=8). betaNHE activity, however, was reduced by 57% and 34% in December 1999 and February 2001, respectively, compared with an otherwise sustained influx that averaged 110.4 +/- 2.3 mmol l(-1) RBCs h(-1) (N=119). Only one reduction coincided with a spawning period but both were preceded by transient increases in circulating testosterone. betaNHE activity measured under standard conditions was not correlated with the number or affinity of beta-ARs nor with water temperature, but both beta-AR numbers and betaNHE activity were positively related to their respective mRNA levels (P=0.005 and 0.038, respectively). Pharmaceutical intervention in the transduction cascade linking the beta-AR and betaNHE failed to indicate any failure of the transduction elements in RBCs displaying low betaNHE activity. Similarly, we failed to demonstrate any link between seasonal cortisol fluctuations and seasonally reduced betaNHE activity. However, the betaNHE activity of age-separated RBC fractions showed that younger RBCs had a significantly higher betaNHE response than older RBCs, consistent with the seasonal reductions in betaNHE being linked to turnover of RBCs and erythropoiesis. Testosterone is known to induce erythropoiesis and we conclude that seasonal reductions in betaNHE are not caused by changes in beta-AR numbers but may be linked to testosterone-induced erythropoiesis.