Involvement of the autonomic nervous system in the in vivo TRH-induced increases in the plasma levels of glucagon, insulin and glucose in rabbits.

Abstract

Thyrotropin-releasing hormone, TRH, increases the plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits. However, TRH has no direct effects on the release of hormones neither from the endocrine pancreas in humans nor from the isolated perfused rat pancreas. The aim of the present study was to investigate if the effects of TRH in rabbits were mediated by the autonomic nervous system. The TRH "Roche"-induced hyperglucagonemia was inhibited by phentolamine (an alpha-receptor blocking drug), yohimbine (an alpha-2 -receptor blocking drug) and atropine. The TRH "Roche"-induced hyperinsulinemia was inhibited by propranolol (a beta-receptor blocking drug). The TRH "Roche"-induced hyperglycemia was inhibited by all four drugs. The TRH "Roche"-induced increases in the plasma levels of free fatty acids were not inhibited by the sympathetic and parasympathetic blocking drugs. The effects of TRH "Roche" on the plasma levels of glucagon, insulin and glucose cannot be explained by increases in the plasma levels of catecholamines. TRH, given intravenously into rabbits, may possibly act on regions in the central nervous system which control carbohydrate metabolism and the release of glucagon and insulin from the endocrine pancreas by sympathetic and parasympathetic mechanisms.