The involvement of the cholinergic system in GH secretion has recently acquired increasing importance. Data have been presented suggesting that in rats the effect of cholinergic modulation on GH secretion takes place through inhibition or stimulation of hypothalamic somatostatin (SRIF) release. To investigate further the significance of cholinergic-SRIF link and its role in the regulation of GH secretion, the action of cholinergic agonist and antagonist drugs in the GH short-loop feedback mechanism mediated by SRIF was investigated. Intracerebroventricular (i.c.v.) infusion of 0·2 or 2·0 μg GH/rat into the lateral brain ventricle of adult male rats induced a significant reduction in the GH-releasing hormone (GHRH; 2 μg/kg, i.v.)-induced peak GH rise, but only the 2·0 μg dose reduced also the GH-integrated area after administration of GHRH. This effect was absent after central administration of 20·0μg GH/rat, due probably to leakage of some GH from the cerebral ventricle into the systemic circulation. Pretreatment with cysteamine (300 mg/kg, s.c.), a known depletor of hypothalamic SRIF, or with anti-SRIF serum (0·5 ml/rat) completely counteracted the lessening of the GH response to GHRH induced by 2·0μg GH injected i.c.v. Similarly, pretreatment with the cholinergic agonist pilocarpine (3 mg/kg, i.v.) completely antagonized the inhibitory effect of central infusion of GH on the GHRH-induced GH response. Atropine (1·0 mg/kg, i.v.), a muscarinic cholinergic antagonist, strikingly inhibited the GHRH-induced GH rise, but when given in combination with i.c.v. infusion of GH there was no additive inhibitory effect. These data reinforce the idea that the GH autofeedback triggered by i.c.v. infusion of GH is mediated by enhanced SRIF release, and suggest that the hypothalamic cholinergic system plays a major role in this mechanism.
J. Endocr. (1988) 117, 273–281
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