AJP - Endocrinology and Metabolism, Vol 251, Issue 3 316-E321, Copyright © 1986 by American Physiological Society
Beta-adrenergic agonists increase amplitude of LH release in orchidectomized rats
S. L. Petrovic, J. C. Bedran De Castro and S. M. McCann
The role of intravenously (iv) injected adrenergic agonists in the
pulsatile secretion of luteinizing hormone (LH) was examined in
unanesthesized, freely behaving, castrated male rats. The alpha
2-adrenergic receptor agonist, clonidine (25 micrograms/kg), and the alpha
1-adrenergic agonist, (-)-phenylephrine (12.5 micrograms/kg), did not
significantly alter pulsatile release of LH. The physiological beta
2-adrenergic receptor agonist, (-)-epinephrine (2.5 micrograms/kg),
significantly increased the mean plasma concentrations of plasma LH and the
amplitude of the LH pulses over a period of 70 min. The specific beta
2-receptor agonist, salmefamol, significantly increased the mean plasma
concentrations of LH and especially the average amplitude of LH pulses over
70-80 min in a dose-related fashion following the injection of doses from
25 to 125 micrograms/kg. The frequency of LH pulses was not significantly
increased by either agonist at any of the doses employed.
Salmefamol-induced increases in plasma LH could be prevented by the
beta-adrenergic blocker, bornaprolol (FM-24), in a dose-related manner.
When injected together with synthetic LH-releasing hormone (400 ng/kg),
salmefamol (125 micrograms/kg) significantly increased the mean plasma
concentrations of LH over 70 min compared with values in controls receiving
LH-releasing hormone only. The data support the concept that beta-agonists
act on their receptors in the pituitary to facilitate LH-releasing
hormone-induced discharge of LH.
