329 THE DEVELOPMENT OP CHOLINERGIC CONTROL OF GROWTH HORMONE (GH) SECRETION

Abstract

As in man, acetylcholine stimulates GH release in adult sheep. The ontogeny of GH stimulation by cholinergic (muscarinic) agonists was studied in chronically catheterized fetal (term 147 days) and infant lambs. The cholinesterase inhibitor (CEI), physostigmine (PHY,100ug/kg) given iv to 11 fetuses between 81 and 138 days gestation with a mean basal GH of 97.7±23.3 ng/ml did not affect fetal plasma GH. In contrast, in 6 infants (3-22 days), PHY stimulated GH from 10.3±1.7 ng/ml to 37.8±8.9 ng/ml (p<0.05) with the maximum response at 30 min. This response was abolished by pretreatment with atropine (AT,100ug/kg iv),(n=3), demonstrating the muscarinic action of PHY on GH release. AT, alone had no effect on GH release (n=3). Neostigmine (120ug/kg iv), a CEI which does not pass the blood-brain barrier (BBB) also stimulated GH release in 3 infants and this effect was abolished by AT (n=3). This suggests that the site of action of cholinergic agonists on GH release is outside the BBB, probably at the pituitary. The late development of the GH response to PHY may represent either the development of cholinergic receptors or cholinesterase in the neonatal pituitary. The development of cholinergic stimulated GH release is in marked contrast to the regulation of GH by serotonin, dopamine, opiates and GABA which develop by 100 days gestation, and is surprising in view of the early appearance of acetylcholine in the fetal brain.

Supported by the Medical Research Council of New Zealand.

Log in or create a free account to read this content

Gain free access to this article, as well as selected content from this journal and more on nature.com

Access through your institution

or

Sign in or create an account

Continue with Google

Continue with ORCiD