Role of the autonomic nervous system in hyperglucagonemia of rats with carbon tetrachloride-induced hepatic injury

Abstract

There are many hypotheses in the mechanism of hyperglucagonemia in humans during cirrhosis or hepatic coma. We studied the effect of receptor blokers to autonomic nervous system on level of plasma glucagon immunoreactivity (GI) in rats given carbon tetra chloride. Administration of propranolol, a betaadrenergic antagoinst, significantly lowered the high level of plasma GI induced by carbon tetrachloride in rats to about 60% of that of controls (p<0.01). Atropine, an anticholinergic agent, also depressed the hyperglucagonemia to about 55% of not-treated animals (p<0.01). The minimum doses of propranolol and atropine to rats on depression of the hyperglucagonemia appeared to be 0.2 and 0.5mg per kg body weight, respectively. On the other hand, phentolamine, an alpha-adrenergic blocker, did not influence the hyperglucagonemia induced by carbon tetrachloride. The concentrations of glucose, immunoreactive insulin, GOT and GPT in plasma were not affected by both propranolol and atropine and these two blockades showed no changes in plasma GI level in normal rats. These results suggest that beta-receptor of sympathetic and cholinergic nervous system might be involved in the process of hyperglucagonemia induced by hepatic failure such as carbon tetrachloride.