Premium
Modulation by somatostatin of nerve‐mediated activation of glycogenolysis in the perfused rat liver
Author(s) -
Beckh Karlheinz,
Ehlenz Klaus,
Arnold Rudolf
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)80752-5
Subject(s) - somatostatin , medicine , endocrinology , glycogenolysis , chemistry , glucagon , neurotransmitter , stimulation , postsynaptic potential , biology , glycogen , central nervous system , receptor , insulin
Perivascular nerve stimulation of rat livers perfused in situ with erythrocyte‐free Krebs‐Henseleit buffer at constant pressure in a non‐recirculating system resulted in an increase of glucose and lactate production and in a decrease of portal flow. Infusion of somatostatin in different concentrations (2 × 10 −7 , 10 −8 , 10 −9 mol·l −1 ) reduced the nerve‐mediated activation of glucose release maximally to 66%. There was only a slight effect on the lactate output, the nerve‐mediated reduction of portal flow was unaltered. In controls, somatostatin alone had no effect on the metabolic and hemodynamic parameters. In order to differentiate between a presynaptic and postsynaptic mechanism, the noradrenaline overflow was calculated. The unaltered release of the neurotransmitter in the presence or absence of somatostatin excluded a presynaptic mechanism. To mimic the nerve effects on the carbohydrate metabolism and on the hemodynamics, noradrenaline (2 × 10 −7 mol·l −1 ) was infused instead of the nerve stimulation over a period of 5 min. Somatostatin did not change the endocrine effects of the catecholamine under these conditions. The nerve‐dependent effect of somatostatin suggests that other neurotransmitters (e.g. VIP) or mediators (e.g. prostanoids) may be influenced by somatostatin.