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This study was designed to elucidate which hormone is responsible for the induction of GH and PRL receptors in rat liver. Intact female rats were implanted with osmotic minipumps delivering rat GH (rGH) or ovine GH (oGH) or PRL at various rates from 75 to 800 micrograms/day for 7 days, and binding of radioiodinated bovine GH or ovine PRL (oPRL) tracer was measured on liver microsomal membranes. MgCl2 treatment was used to remove bound hormones from receptors before tracer binding. Infusion of rGH resulted in a significant increase (P less than 0.001) in both GH and PRL binding, the effect being maximal (2.5- to 3-fold for both ligands) at rGH infusion rates from 150 to 400 micrograms/day. Serum rGH levels were elevated 3- to 5-fold in these animals, but somatomedin-C concentrations were not higher than in controls. MgCl2 treatment showed that GH, but not PRL, binding sites in rGH-treated animals were significantly occupied by administered hormone. Analysis of competitive binding curves indicated that receptors for both GH and PRL increased in concentration without changes in binding affinity. In contrast to the rGH effect, oGH infusion from 75 to 400 micrograms/day failed in two experiments to consistently alter either bovine GH or oPRL binding sites. This was not explained by the potency of the preparation at the somatogenic receptor; oGH was in fact more potent than rGH. The effects of rat PRL and oPRL infusion on receptor levels were also assessed. In contrast to previous reports, neither preparation caused induction of either PRL or GH binding sites. oPRL decreased PRL binding by 30-40% when infused between 200 and 400 micrograms/day, whereas rat PRL had a less consistent effect. MgCl2 stripping of membranes suggested that administered PRL preparations did not significantly occupy PRL receptors. GH receptors were unaffected in any PRL-treated group. It is concluded that in intact female rats, rGH regulates the concentration of both GH and PRL receptors. The slight down-regulation of PRL receptors resulting from PRL infusion casts further doubt on the concept that PRL induces its own hepatic receptors.
R C Baxter, and
Z Zaltsman, and
J R Turtle
January 1993,
Virchows Archiv. A, Pathological anatomy and histopathology,
R C Baxter, and
Z Zaltsman, and
J R Turtle
October 1995,
Molecular and cellular endocrinology,
R C Baxter, and
Z Zaltsman, and
J R Turtle
February 1995,
Molecular and cellular endocrinology,
R C Baxter, and
Z Zaltsman, and
J R Turtle
February 1989,
The Anatomical record,
R C Baxter, and
Z Zaltsman, and
J R Turtle
October 1982,
Pharmacology, biochemistry, and behavior,
R C Baxter, and
Z Zaltsman, and
J R Turtle
November 1999,
Endocrinology,
R C Baxter, and
Z Zaltsman, and
J R Turtle
January 1979,
International journal of neurology,
R C Baxter, and
Z Zaltsman, and
J R Turtle
January 2008,
Acta neurochirurgica. Supplement,
R C Baxter, and
Z Zaltsman, and
J R Turtle
April 1978,
Psychoneuroendocrinology,
R C Baxter, and
Z Zaltsman, and
J R Turtle
January 1986,
Neuroendocrinology,
