In Rana sylvatica, freeze-induced liberation of glucose from hepatic glycogen stores plays a critical role in conferring freeze tolerance. To determine whether an alteration in hepatic adrenergic receptor status, which dictates catecholamine-directed hepatic glycogenolytic responses, is involved in the glycemic response to freezing, hepatic α1 α2, and β2 adrenergic receptors and calcium transport were characterized by radioligand and radioisotopic techniques, respectively, in plasma membranes isolated from the livers of control, −2.5 °C-exposed, and frozen–thawed frogs. The three adrenergic receptors display marked and different patterns of changes in response to freezing, with two distinct receptor shifts clearly evident. In the control state, the β2 adrenergic receptor dominates over the α1 receptor. At 12 h, β2 adrenergic receptor dominance intensifies by a receptor shift involving a decrease in the α1 and α2 adrenergic receptors. Coincident with the initiation of the glycemic response, this early shift may be causally related to it. At 24 h, the α1 adrenergic receptor dominates, achieved by a receptor shift involving a decrease in the β2 adrenergic receptor and an increase in the α1 and α2 adrenergic receptors. This shift may be related to the maintenance of the glycemic response. Receptor shifts are associated with changes in calcium transport, which accentuate them. The thawed state is characterized by recovery of α, but not β2, receptor expression correlatable with, and perhaps allowing, a switch to hepatic glycogenesis. The role of thyroid hormone, whose levels are lower in the frozen state, in inducing receptor shifts is discussed.Key words: hepatic adrenergic receptors, Rana sylvatica, freeze tolerance, glycemic response, thyroid hormones.
Enteral tranexamic acid attenuates vasopressor resistance and changes in α1-adrenergic receptor expression in hemorrhagic shock