The role of acetylcholine (Ach) in the regulation of human GH secretion was assessed using atropine, which selectively blocks cholinergic muscarinic receptors. Paired tests were performed in seven normal subjects using GH-releasing hormone (GHRH) 1-44 (1 μg/kg iv), with and withot atropine pretreatment (1 mg im). The GHRH 1-44-induced GH secretory peak [20.7 ± 4.5 (SEM) ng/ml] was completely blocked by atropine administration (2.3 ± 0.6 ng/ml) (P < 0.01). To determine whether this atropine blockade was at the pituitary level, a series of in vitro studies were conducted using monolayer cultures of cells from bovine anterior pituitary glands. GHRH 1-44 (10-8 M) stimulated bovine GH release (11.1 ± 1.5 μg/ml) as compared to control values (5.1 ± 0.4 μg/ml) (P < 0.01). This response was not altered by 10-6 M atropine (14.9 ± 0.9 μg/ml). Similar results were obtained with GHRH, 10-9 M, with or without atropine, 10-7 M. Addition of 10-6 M Ach to the incubation medium significantly increased bovine GH release (12.7 ± 1.2 μg/ml) and the effect of 10-6 M Ach and 10-8 M GHRH was additive (20.9 ± 2.1 μg/ml) (P < 0.01). Similar results were obtained with Ach, 10-5 M, and GHRH, 10-9 M. Atropine or eserine alone did not alter basal GH secretion, and atropine blocked Ach-stimulating activity. In conclusion, atropine blockade of GHRH-induced GH secretion appears to be exerted at a site other than pituitary.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Clinical Biochemistry
- Biochemistry, medical