ALTERATIONS IN HEPATIC ADRENERGIC-RECEPTOR STATUS IN RANA-SYLVATICA IN RESPONSE TO FREEZING AND THAWING - IMPLICATIONS TO THE FREEZE-INDUCED GLYCEMIC RESPONSE
Sj. Hemmings et Kb. Storey, ALTERATIONS IN HEPATIC ADRENERGIC-RECEPTOR STATUS IN RANA-SYLVATICA IN RESPONSE TO FREEZING AND THAWING - IMPLICATIONS TO THE FREEZE-INDUCED GLYCEMIC RESPONSE, Canadian journal of physiology and pharmacology, 72(12), 1994, pp. 1552-1560
In Rana sylvatica, freeze-induced liberation of glucose from hepatic g
lycogen stores plays a critical role in conferring freeze tolerance. T
o determine whether an alteration in hepatic adrenergic receptor statu
s, which dictates catecholamine-directed hepatic glycogenolytic respon
ses, is involved in the glycemic response to freezing, hepatic alpha(1
), alpha(2), and beta(2) adrenergic receptors and calcium transport we
re characterized by radioligand and radioisotopic techniques, respecti
vely, in plasma membranes isolated from the livers of control, -2.5 de
grees C-exposed, and frozen-thawed frogs. The three adrenergic recepto
rs display marked and different patterns of changes in response to fre
ezing, with two distinct receptor shifts clearly evident. In the contr
ol state, the beta(2) adrenergic receptor dominates over the alpha(1)
receptor. At 12 h, beta(2) adrenergic receptor dominance intensifies b
y a receptor shift involving a decrease in the alpha(1) and alpha(2) a
drenergic receptors. Coincident with the initiation of the glycemic re
sponse, this early shift may be causally related to it. At 24 h, the a
lpha(1) adrenergic receptor dominates, achieved by a receptor shift in
volving a decrease in the beta(2) adrenergic receptor and an increase
in the alpha(1) and alpha(2) adrenergic receptors. This shift may be r
elated to the maintenance of the glycemic response. Receptor shifts ar
e associated with changes in calcium transport, which accentuate them.
The thawed state is characterized by recovery of alpha but not beta(2
), receptor expression correlatable with, and perhaps allowing, a swit
ch to hepatic glycogenesis. The role of thyroid hormone, whose levels
are lower in the frozen state, in inducing receptor shifts is discusse
d.