ALTERATIONS IN HEPATIC ADRENERGIC-RECEPTOR STATUS IN RANA-SYLVATICA IN RESPONSE TO FREEZING AND THAWING - IMPLICATIONS TO THE FREEZE-INDUCED GLYCEMIC RESPONSE

Citation
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
Citations number
79
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
00084212
Volume
72
Issue
12
Year of publication
1994
Pages
1552 - 1560
Database
ISI
SICI code
0008-4212(1994)72:12<1552:AIHASI>2.0.ZU;2-J
Abstract
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.