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  • Title: Modulation by somatostatin of nerve-mediated activation of glycogenolysis in the perfused rat liver.
    Author: Beckh K, Ehlenz K, Arnold R.
    Journal: FEBS Lett; 1989 Jul 03; 250(2):345-8. PubMed ID: 2568947.
    Abstract:
    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 x 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 x 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.
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