title: Pharmacological evidence for stimulation of growth hormone secretion by a central noradrenergic system in dogs.
abstract: The role of brain catecholamines in the regulation of growth hormone secretion was investigated in pentobarbital-anesthetized dogs by using drugs which modify the function of adrenergic neurons and receptors. Intravenous administration of L-dopa produced a prompt, statistically significant increase in plasma growth hormone concentration. This response was not significantly reduced by blockade of peripheral dopa decarboxylase activity with carbidopa. Clonidine, an alpha-agonist which penetrates the brain, increased plasma growth hormone secretion. Norepinephrine, epinephrine, dopamine and isoproterenol, catecholamines which do not penetrate the blood-brain barrier, failed to affect plasma growth hormone concentration when administered intravenously. Apomorphine did not produce a statistically significant increase in plasma growth hormone concentration when administered directly into the the third ventricle, and pimozide failed to abolish the increase in plasma growth hormone produced by L-dopa. The increase in plasma growth hormone concentration produced by intravenous L-dopa and clonidine was prevented by administration of phentolamine or phenoxybenzamine directly into the third ventricle. The response to L-dopa was also abolished by intraventricular procaine. In dogs in which central beta-adrenergic blockade was produced by intraventricular L-propranolol, the growth hormone response to L-dopa was greater than it was in control dogs treated with intraventricular D-propranolol. The data indicate that in pentobarbital anesthetized dogs, the increase in growth hormone secretion produced by L-dopa is mediated by norepinephrine, rather than dopamine, that the site of action of the norepinephrine is central, above the median eminence and inside the 'blood-brain barrier', and that the norepinephrine acts via alpha-adrenergic receptors.
authors.affiliation: Departments of Physiology and Pediatrics, University of California, San Francisco, CA 94143, USA.
authors.forename: R
authors.initials: R
authors.lastname: Lovinger
authors.forename: J
authors.initials: J
authors.lastname: Holland
authors.forename: S
authors.initials: S
authors.lastname: Kaplan
authors.forename: M
authors.initials: M
authors.lastname: Grumbach
authors.forename: A T
authors.initials: AT
authors.lastname: Boryczka
authors.forename: R
authors.initials: R
authors.lastname: Shackelford
authors.forename: J
authors.initials: J
authors.lastname: Salmon
authors.forename: I A
authors.initials: IA
authors.lastname: Reid
authors.forename: W F
authors.initials: WF
authors.lastname: Ganong
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002230:Carbidopa / Q000494:pharmacology; D002395:Catecholamines / Q000494:pharmacology; D003000:Clonidine / Q000494:pharmacology; D004285:Dogs; D015259:Dopamine Agents / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D013006:Growth Hormone / Q000097:blood / Q000187:drug effects / Q000378:metabolism*; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000378:metabolism*; D007276:Injections, Intraventricular; D007980:Levodopa / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism*; D010868:Pimozide / Q000494:pharmacology; D011941:Receptors, Adrenergic / Q000187:drug effects / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000378:metabolism*
chemical_list: D000317:Adrenergic alpha-Antagonists; D002395:Catecholamines; D015259:Dopamine Agents; D018492:Dopamine Antagonists; D011941:Receptors, Adrenergic; D010868:Pimozide; D007980:Levodopa; D013006:Growth Hormone; D003000:Clonidine; D002230:Carbidopa; D001058:Apomorphine; D009638:Norepinephrine