Adrenergic modula tion of insulin secretion in response to portal glucose and arginine in the ra t

It has been suggested that there are hepatic receptors for sodium chloride 1) glucose 2,3), amino acids 4-7), and osmotic pressure 8) Several studies have shown that the receptors for glucose or arginine in the hepato-portal system exert a reflex regulation of the pancreatic neuroendocrine system and modulate insulin secretion 2,4-6,9) The vagal efferent pathways may be involved in the pancreatic neuroendocrine system via the afferent pathways from the hepatic neural metabolic receptors. Thus, hepatic glucose receptor is suggested to stimulate insulin secretion 2) and hepatic arginine receptor is suggested to inhibit insulin secretion via cholinergic mechanisms 4,6) However, the neural modulation of hepato-portal glucose-or arginine-receptors in insulin secretion remains to be fully elucidated. In order to clarify this issue, the effect of cholinergic blockade or adrenergic blockade on insulin secretion in response to intraportal glucose or arginine was investigated in the rat.