Endocrinology, Vol 100, 792-798, Copyright © 1977 by Endocrine Society
Further evidence for inhibition of episodic luteinizing hormone release in ovariectomized rats by stimulation of dopamine receptors
SV Drouva and RV Gallo
Department of Physiology, University of California, School of Medicine, San Francisco 94143.
Stimulation of dopamine receptors by apomorphine inhibits episodic LH
release in ovariectomized rats. The present study was designed to examine
further the role of dopamine in this process. Unrestrained, unanesthetized
rats with indwelling right atrial cannulae were bled continuously (30 or 50
microliters of whole blood/5 min for 3-6 h) and whole blood samples
analyzed for LH by radioimmunoassay. Animals were treated with various
compounds reported to stimulate or block dopamine receptors. ET 495, a long
acting dopamine receptor stimulating agent, caused a marked inhibition of
episodic LH release (2 1/2-4 h). Control injections of distilled water had
no effect. d-Butaclamol, a blocker of dopamine receptors, did not itself
alter episodic LH release but prevented the inhibitory effects seen
following apomorphine or ET 495. I-butaclamol, a biologically inactive form
of butaclamol, had no effect. Measurement of plasma corticosterone levels
in these same animals indicated increased values following apomorphine or
ET 495 alone (when LH release was inhibited), as well as after apomorphine
or ET 495 administration to d-butaclamol-pretreated rats (when LH levels
did not change). These data support our previous hypothesis that in
ovariectomized adult rats, activation of dopamine receptors is capable of
inhibiting episodic LH release, but that dopamine may not play an
inhibitory role under normal physiological conditions in the modulation of
LH secretion. In addition, the inhibitory action of apomorphine and ET 495
does not appear to be exerted via a stress-induced release of adrenal
corticosterone.
