Influence of the thyroid status on the hepatic [alpha]1
-adrenoreceptor responsiveness.
Daza, Francisco J., Roberto Parrilla, and Angeles Mart[acute]in
-Requero.
Department of Physiophathology and Human Molecular Genetics, Centro
de Investigaciones Biol[acute]ogicas (CSIC), Vel[acute]azquez 144,
28006-Madrid, SPAIN
APStracts 4:0168E, 1997.
The present work aimed to elucidate the influence of the thyroid
functional status on the [alpha]1-adrenoreceptor-induced activation
of hepatic metabolic functions. The experiments were performed in
either a non-recirculating liver perfusion system featuring
continuous monitoring of portal pressure, pO2, pCa2+, pH, or isolated
hepatocytes from euthyroid, hyperthyroid, and hypothyroid rats.
Hypothyroidism decreased the [alpha]1-adrenergic stimulation of
respiration, glycogen breakdown and gluconeogenesis. These effects
were accompanied by a decreased intracellular Ca2+ mobilization
corroborating that those processes are regulated by the Ca2+
dependent branch of the [alpha]1-adrenoreceptor signaling pathway.
Moreover, in hyperthyroid rats the [alpha]1-adrenergic-induced
increase in cytosolic Ca2+ was enhanced and glucose synthesis or
mobilization were not altered.
The thyroid status influenced neither the [alpha]1-adrenergic
stimulation of vascular smooth muscle contraction nor the [alpha]1
-agonist-induced intracellular alkalinization and protein kinase C
(PKC) activation. Thus, the distinct impairment of the Ca2+-dependent
branch of the [alpha]1-adrenoreceptor signaling pathway by thyroid
status provides a useful tool to investigate the role played by each
signaling pathway, Ca2+ or PKC, in controlling the hepatic functions.
Received 14 March 1997; accepted in final form 24 July 1997.
APS Manuscript Number E117-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 27 August 1997