Studies of anterior pituitary-grafted rats: I. Abnormal prolactin response to thyrotropin releasing hormone, clonidine, insulin, and fasting.
Although the rat implanted with extra anterior pituitary glands (AP) under the kidney capsule has been widely used as a model of chronic hyperprolactinemia, its hormonal status has not been fully characterized. Using conscious, unrestrained female pituitary-grafted rats and sham-operated littermates, we investigated prolactin (PRL) secretion in response to the following stimuli: thyrotropin releasing hormone (TRH), clonidine, insulin, and fasting. The AP-implanted rats had a greater and more sustained rise in serum PRL after TRH than control rats, reflecting a direct effect of TRH on the ectopic lactotropes. In contrast after clonidine, which acts via the hypothalamus, the serum PRL rose to much higher levels in sham-operated rats than in rats bearing ectopic pituitary tissue. Both insulin-induced hypoglycemia and fasting decreased serum PRL in control rats, but the AP-implanted animals manifested a rise in serum PRL in response to these stimuli. Thus, the AP-implanted rat is not only a valid model of excess and abnormal PRL secretion, but it may also be useful for distinguishing between stimuli requiring an intact hypothalamic-pituitary unit and agents which act directly on the pituitary gland.
D000818:Animals; D003000:Clonidine / Q000494:pharmacology*; D005215:Fasting; D005260:Female; D007003:Hypoglycemia / Q000097:blood; D007328:Insulin / Q000494:pharmacology*; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000637:transplantation*; D011388:Prolactin / Q000097:blood*; D051381:Rats; D011919:Rats, Inbred Strains; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology*
D007328:Insulin; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D003000:Clonidine