Further Evidence for Inhibition of Episodic Luteinizing Hormone Release in Ovariectomized Rats by Stimulation of Dopamine Receptors1

Abstract

Stimulation of dopamine receptors by apomorphine inhibits episodic LH [luteinizing hormone] release in ovariectomized rats. The role of dopamine in this process was further examined. Unrestrained, unanesthetized rats with indwelling right atrial cannulae were bled continuously (30 or 50 .mu.l 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 [piribedil methane sulfonate] a long acting dopamine receptor stimulating agent, caused a marked inhibition of episodic LH release (2 1/2-4 h). Control injections of distilled H2O 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. l-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), and after apomorphine or ET 495 administration to d-butaclamol-pretreated rats (when LH levels did not change). These data support the 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. The inhibitory action of apomorphine and ET 495 does not appear to be exerted via a stress-induced release of adrenal corticosterone.