Islet Neurotransmitters Sympathetic Effects

It was initially thought that the neurotransmitter mediating the sympathetic effects is norepinephrine because this is the classic adrenergic neurotransmitter and is known to inhibit glucose stimulated insulin secretion.70 However, combined adrenergic blockade does not abolish the influences of sympathetic nerve stimulation on insulin and glucagon secretion and norepinephrine only partially reproduces the stimulation of glucagon secretion that accompanies sympathetic nerve activation.71'72 Therefore, the sympathetically induced influences on islet hormone secretion seem to be partially nona-drenergic. Such effects may be mediated by neuropeptides confined to sympathetic nerve terminals, such as NPY73 and galanin.74 This hypothesis is supported by the findings that both NPY and galanin are released from the pancreas during sympathetic nerve stimulation and that both of these neuropeptides inhibit insulin secretion and stimulate glucagon secretion.75 79 In addition, NPY may be involved in the regulation of pancreatic blood flow because perivascular adrenergic nerves contain NPY73 and NPY has profound vasoconstrictor influences on the pancreas.79 Therefore, it is established that sympathetic nerve activation inhibits insulin but stimulates glucagon secretion, although the neurotransmitter involved on these actions has not been finally defined. It is tempting to speculate that different neurotransmitters are involved under different conditions in the sympathetic regulation of islet function. For example, the inhibition by sympathetic nerve activation of basal insulin secretion might be mediated by a neuropeptide (NPY, galanin, or both), whereas the inhibition of glucose-stimulated insulin secretion might be mediated by norepinephrine.

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