Premium
Functional Interrelationships Between Adrenergic and Opioid Systems in the Neuroregulation of Growth Hormone Secretion in Infant Rats
Author(s) -
Arce Victor M.,
Cella Silvano G.,
Locatelli Vittorio,
Müller Eugenio E.
Publication year - 1991
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1991.tb00287.x
Subject(s) - clonidine , endocrinology , medicine , yohimbine , (+) naloxone , agonist , basal (medicine) , opioid , opioid peptide , receptor , antagonist , insulin
Functional interrelationships between hypothalamic adrenergic and opioid systems were studied in 10‐day‐old male and female rats. Either clonidine (150 μg/kg, sc), an α 2 ‐adrenoceptor agonist, or FK 33‐824 (1 mg/kg, sc), a synthetic analog of met‐enkephalin, increased plasma growth hormone (GH) levels, the increment being significantly higher with FK 33‐824 than with clonidine. Pharmacologic blockade of opioid receptors with naloxone (5 mg/kg, sc) did not modify either basal GH levels, or the GH response to clonidine, whereas blockade of α 2 ‐adrenoceptors with yohimbine (2.5 mg/kg, sc) reduced basal GH levels and partially counteracted the FK 33‐824‐induced GH rise. Clonidine (150μ/kg, sc, twice daily) administered from postnatal day 5 to 9, increased basal GH levels and pituitary GH content. In these pups, acute administration of clonidine failed to further release GH, but the GH response to acute administration of FK 33‐824 was significantly enhanced. A 5‐day treatment with FK 33‐824 (1 mg/kg, sc, twice daily), neither modified basal GH levels, nor pituitary GH content. Under these conditions, the in vivo GH response to an FK 33‐824 challenge was significantly enhanced, and the response to clonidine was preserved. Pituitaries from FK 33‐824‐pretreated rats were hyperresponsive to GH‐releasing hormone (10 −7 M). In summary, our data indicate that in rat pups: 1) two separate components i.e. one adrenergic, the other extra‐adrenergic, subserve the GH‐releasing effect of opioid peptides; 2) in contrast to short‐term stimulation of α 2 ‐adrenoceptors, stimulation of opioid receptors does not trigger GH synthesis or induce down‐regulation or tolerance; 3) short‐term opioid stimulation does not affect an α 2 ‐adrenergic challenge, but sensitizes to an opioid challenge.