Effect of adrenergic-blocking or -stimulating agents on plasma growth hormone, immunoreactive insulin, and blood free fatty acid levels in man

Abstract

In order to determine whether an adrenergic mechanism is involved in the secretion of growth hormone and insulin, the effect of adrenergic-blocking or -stimulating agents on plasma human growth hormone (HGH), immunoreactive insulin, blood free fatty acids (FFA), and glucose levels was studied in normal human subjects. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused a rise in plasma HGH, a transient decrease in blood FFA, and no significant change in plasma insulin. This increase in plasma HGH was inhibited either by the combined administration of isoproterenol, a beta adrenergic-stimulating agent, along with propranolol or by oral glucose loading immediately before the start of propranolol infusion. The concomitant administration of epinephrine and propranolol brought about a rise in plasma HGH comparable with that produced by propranolol alone, without any significant change in blood FFA. Alpha adrenergic blockade by the intravenous infusion of phenotolamine significantly suppressed plasma HGH responses to insulin-induced hypoglycemia and to arginine infusion, and enhanced plasma insulin response to arginine infusion. It also stimulated lipid mobilization significantly. The intravenous infusion of alpha adrenergic-stimulating agents, phenylephrine and methoxamine, caused an increase in plasma HGH, a slight decrease in blood FFA, and no significant change in plasma insulin. This increase in plasma HGH was significantly inhibited by the simultaneous administration of phentolamine along with methoxamine. On the contrary, a beta adrenergic stimulant, isoproterenol, raised plasma insulin and blood FFA, and abolished the plasma HGH response to propranolol. Another beta stimulator, isoxsuprine, raised blood FFA but not plasma insulin. It is concluded that either beta adrenergic blockade or alpha stimulation enhances HGH secretion and inhibits insulin secretion and fat mobilization, whereas either alpha blockade or beta stimulation stimulates insulin secretion and fat mobilization and inhibits HGH secretion.