Prostaglandin F2α Overcomes Blockade of Episodic LH Secretion with Testosterone, Melengestrol Acetate or Asprin in Bulls

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Abstract
Three experiments were conducted to identify inhibitors of episodic LH [luteinizing hormone] release and to determine whether prostaglandin F2.alpha. (PGF2.alpha.) overcomes blockade of LH release in bulls. In the 1st experiment, episodic secretion of LH and testosterone occurred in each of 4 bulls during a 12-h control period. Infusion of testosterone (2.5 mg/h) into a jugular vein to cause blood testosterone concentrations (6-10 ng/ml) equivalent to the maximum normally found completely blocked episodic LH release. Administration of PGF2.alpha. (30 mg, s.c.), 13 h after the start of the testosterone infusion caused release of LH in all 4 bulls; a 2nd injection of PGF2.alpha. at 24 h after beginning of testosterone caused less LH release. When gonadotropin-releasing hormone was given to the same bulls at 32 h of testosterone infusion, a synchronous 6- to 8-fold increase of plasma LH occurred in each bull. In the 2nd experiment, melengestrol acetate (MGA, .5 mg fed twice daily) completely blocked episodic release of LH and testosterone, but administration of PGF2.alpha. overcame this blockade in 4 bulls. Administration of LH to these bulls caused a surge of testosterone equivalent to that in 4 bulls which were not given MGA, so MGA did not inhibit the action of LH on testes. In the final experiment with another 4 bulls, oral administration of aspirin (150 g every 4 h) suppressed episodic release of LH and testosterone and administration of exogenous PGF2.alpha. caused increased blood LH and testosterone in the face of aspirin blockade. Thus, testosterone, MGA and aspirin each abolish episodic release of LH in bulls; these effects may be overcome by administration of PGF2.alpha.. These results support the hypothesis that prostaglandin normally may participate in induction of episodic LH release in bulls and that testosterone may exert negative feedback on LH secretion in bulls by inhibiting prostaglandin-induced release of LH.