Catecholamine involvement in the control of growth hormone secretion in the domestic fowl

Abstract

A neuropharmacologic approach was utilized to investigate the catecholaminergic influence on the hypothalamic regulation of growth hormone (GH) secretion in young (6-week-old) male domestic fowl. The selective inhibition of norepinephrine (NE) and epinephrine (E) synthesis or activity by diethyldithiocarbamate (DDC), FLA63 (dopamine-β-hydroxylase inhibitors), phenoxybenzamine (α 1 receptor blocker), and yohimbine (α 1 and α 2 receptor antagonist) was associated with a decline in circulating GH levels. Similarly inhibition of NE reuptake by imipramine or desmethylimipramine were followed by reduced GH secretion. In the presence of α-methyl- p-tyrosine (αMpt, a tyrosine hydroxylase inhibitor), the administration of phenylephrine (α 1 agonist) was followed by increased plasma concentrations of GH. However, alone, it was without effect. Similarly plasma concentrations of GH were elevated by dihydroxyphenylserine (DOPS, a precursor of NE E ) in chicks pretreated with DDC or carbidopa. These data are consistent with the stimulatory hypothalamic control of GH involving NE E which exert their effects via α (probably α 1) postsynaptic stimulatory receptors. Evidence that it is E rather than NE, which is the catecholamine involved or the hypothalamic control of GH, comes from the decrease in plasma GH concentration following the inhibition of central E synthesis by SKF64139 (an inhibitor of phenylethanolamine- N-methyltransferase). Some evidence for a limited inhibitory dopaminergic system was found. Inhibition of dopamine (DA) synthesis by αMpt produced significant elevations in plasma GH concentration. In addition, apomorphine (DA agonist) consistently depressed GH release. However, blockade of DA receptors by pimozide had either no effect on plasma GH concentrations or at a very high dose decreased plasma GH concentrations. NE E also appear to have a depressive effect on plasma concentrations of GH in young chicks, probably via a peripheral site of action. Plasma concentrations of GH were reduced by the peripheral administration of NE, which might be expected not to cross the blood-brain-barrier (BBB), α 1 α 2 agonists clonidine and p-amino clonidine (which does not cross BBB), NE E precursors l-DOPA and DOPS, and the β agonist, isoproterenol. Furthermore, the depression of peripheral E synthesis (by SKF29661 which inhibits phenylethamolamine- N-methyltransferase) elevated the plasma concentration of GH.