J. Biol. Chem., Vol. 257, Issue 23, 13907-13910, Dec, 1982
Stimulation of hepatic glycogenolysis by alpha 1- and beta 2-adrenergic agonists. Evidence against short term agonist-induced desensitization of the responses
NG Morgan, EA Shuman, JH Exton and PF Blackmore
Addition of alpha 1-adrenergic agonists or vasopressin to the medium
perfusing rat livers was associated with a rapid efflux of Ca2+, which was
rapidly reaccumulated on removal of the stimulus. The magnitudes of the
respective Ca2+ efflux and influx responses were similar, suggesting that
Ca2+ was being mobilized from, and then reaccumulated into, the same
pool(s). Addition of combinations of alpha 1-agonists, vasopressin and
angiotensin II to isolated hepatocytes revealed that the Ca2+ efflux
response induced by each individual hormone could only be augmented by
addition of a second hormone when submaximal doses of each were employed.
This suggests that an identical pool(s) of hepatocyte Ca2+ is mobilized in
response to each of these agents. No desensitization of the alpha
1-adrenergic glycogenolytic response was observed in the perfused liver,
upon repeated or more prolonged (25 min) exposure to agonist, providing
cell Ca2+ reaccumulation occurred before addition of each successive
stimulus. Selective short term stimulation of the beta 2-adrenergic
glycogenolytic response in immature male rats (less than 150 g, body
weight) was not associated with desensitization to subsequent stimulation.
These data demonstrate that the glycogenolytic response of liver cells does
not become desensitized by successive short term stimulation with alpha 1-
or beta 2-adrenergic agonists.
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