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Perifusion of rat hemipituitaries was used as an in vitro model for luteinizing hormone (LH) release in response to gonadotropin-releasing hormone (GnRH). LH release during continuous stimulation with GnRH (10(-7) M) was inhibited by EGTA (1.5 or 5 mM given 1 h prior to GnRH) or by D-600 (methoxyverapamil, 1 mM, given concomitantly with GnRH). These findings suggested that GnRH-stimulated LH release was a Ca2+-dependent process. Inhibition of LH release caused by Ca2+ chelation with EGTA was reversed when hemipituitaries were returned to medium without EGTA. Elevation of medium K+ (to 50 mM, without GnRH) stimulated Ca2+-dependent LH release during the 1st h. GnRH-stimulated LH release was 60% inhibited by cycloheximide (25 micrograms/ml) after the 1st h. LH release was not stimulated by dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP), although this cyclic nucleotide was shown to have biological activity and to enter pituitary cells as judged by its ability to stimulate prolactin release from the same tissue. The data suggest that optimal LH release in response to GnRH requires extracellular Ca2+ and depends on protein synthesis.
J E Stern, and
P M Conn
December 1984,
Experientia,
J E Stern, and
P M Conn
January 1997,
Life sciences,
J E Stern, and
P M Conn
December 1985,
The American journal of physiology,
J E Stern, and
P M Conn
May 1973,
FEBS letters,
J E Stern, and
P M Conn
July 1993,
Endocrinology,
J E Stern, and
P M Conn
June 1993,
Neuroendocrinology,
J E Stern, and
P M Conn
December 1986,
The Journal of experimental zoology,
J E Stern, and
P M Conn
July 1991,
Domestic animal endocrinology,
J E Stern, and
P M Conn
January 1979,
Neuroendocrinology,
J E Stern, and
P M Conn
January 2009,
Molecular and cellular endocrinology,
