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Evidence for Noradrenergic Involvement in Episodic Prolactin and Growth Hormone Release in Ovariectomized Rats^*

A. NEGRO-VILAR, S. R. OJEDA, J. P. ADVIS and S. M MCCANN

Department of Physiology, University of Texas Health Science Center Dallas, Texas 75235

Address requests for reprints to: Dr. Andres Negro-Vilar, Department of Physiology, University of Texas Health Science Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235

Abstract

Episodic release of PRL and GH was studied in conscious ovariectomized (OVX) rats. Three to 5 weeks after OVX, animals bearing indwelling jugular cannulae were bled at 10-min intervals for 2 h, usually between 1100–1500 h. All animals showed frequent secretory bursts of PRL and GH. PRL levels varied from trough values of 5–10 ng/ml to peak concentrations ranging from 20–65 ng/ml. GH levels fluctuated from baseline values of around 15 ng/ml to peak levels higher than 40 ng/ml in all animals studied (range, 45–205 ng/ml). In another group of animals, norepinephrine (NE) synthesis was inhibited by administering diethyldithiocarbamate (DDC), an inhibitor of dopamine-β-hydroxylase, 2 h before the bleeding period. After this treatment, complete suppression of both PRL and GH secretory episodes was observed. Effectiveness of the DDC treatment was ascertained by measuring the content of NE and dopamine in the median eminence, medial basal hypothalamus, and suprachiasmatic-preoptic area by radioenzymatic assay. At 4 h after DDC injection, NE levels in all three areas were significantly reduced, whereas dopamine levels were not affected.

Stimulation of -adrenergic receptors with clonidine in DDCtreated rats induced a small rise in PRL levels and a distinct rise in GH. If the OVX rats were pretreated with estradiol benzoate (20 µg/rat, 48 h before the experiment), the effect of clonidine on PRL release was remarkably potentiated, while the GH response was somewhat diminished. These results indicate that the noradrenergic system plays an important stimulatory role in episodic PRL and GH secretion and also that the actions of NE on PRL and GH secretion may be differentially modulated by estrogens.

Footnotes

^* This work was supported by grants from the NIH (AM-10073 and HD-09988) and the Ford Foundation.

Postdoctoral Research Fellow of the Ford Foundation

Received November 15, 1978.

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