Endocrinology, Vol 98, 451-460, Copyright © 1976 by Endocrine Society
Simulation of the proestrous luteinizing hormone (LH) surge after infusion of LH-releasing hormone in phenobarbital-blocked rats
CA Blake
Four-day cycling rats were kept in a room with the lights on from 0500-
1900 h. Injection of an ovulation-blocking dose of phenobarbital at 1230 h
on proestrus did not alter the rise in plasma LH concentration in response
to rapid injection of 12.4, 124, or 1240 ng of LHRH at 1300 h. In
additional blocked rats, blood was rapidly withdrawen through one of two
indwelling atrial cannulas while LHRH was infused at a constant rate
through the other. Administration of a given amount of LHRH by slow
infusion was much more effective in elevating plasma LH than was rapid
injection of the same amount of releasing hormone. The pattern of plasma LH
concentration after infusion of approximately 50 ng of LHRH per hour from
1500-1810 h was remarkably similar to that of the spontaneous LH surge,
i.e., a gradual rise in plasma LH concentration followed by a steep linear
increase to high levels which remained elevated for a period of
approximately 2 h before declining rapidly soon after the end of infusion.
In rats given a second 3 h infusion of LHRH at the same rate, from 2200 to
0100 h, a different response pattern was seen: the initial increase in
plasma LH was greater, but the linear rise, which ensued after a lag period
of similar duration (about 45 min), was less marked. Prolongation of the
first infusion beyond 1800 h did not prolong the plateau: plasma LH levels
declined before the infusion was terminated. This decline was less rapid
than that seen at the end of a spontaneous LH surge, which in turn was less
rapid than that seen after termination of a 3 h and 10 min infusion
starting at the same time (1500 h), suggesting that both LHRH release and
pituitary responsiveness are diminished (but not abolished) at this time.
These findings clearly indicate that, in phenobarbital-blocked proestrous
rats, the major part of the proestrous LH surge (including rising and
plateau phases) can be simulated by a constant-rate infusion of about 150
ng of LHRH over the 3 h and 10 min period beginning at 1500 h. Since the
data also suggest that LHRH release is reduced and/or occurs sporadically
during the terminal phase of the surge (when plasma LH levels are
declining), these experiments imply that the LH surge is caused by a
properly timed, nearly constant-rate release of LHRH for about 3 h
(beginning about 1500 h of proestrus) followed by a period of diminished
LHRH release.
