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The aim of this study was to examine the regulation of basal pulsatile LH release by ovarian estradiol (E2) and progesterone (P) during the interval between the mornings of proestrus and estrus in the rat estrous cycle. Pulsatile LH release was studied in six groups of rats bled continuously through jugular venous cannulae between 0930-1230 h at a rate of 50 microliter whole blood/5 min: 1) bled on proestrus; 2) sham ovariectomy (OVX) at 0900-1000 h on proestrus and bled on estrus; 3-6) OVX at 0900-1000 h on proestrus, implanted with either empty or E2-, P-, or E2- plus P-containing Silastic capsules, and bled 24 h after OVX. In our colony, plasma E2 levels peaked at 1300 h, remained high through 1730 h, and then declined. Plasma P values increased between 1300 and 1730 h, peaked at 2000 h, and were rapidly declining by 2400 h. To reproduce the magnitude as well as the temporal pattern for these changes in plasma E2 and P levels, E2 capsules were inserted at the time of OVX on proestrus and removed at 1830 h. P capsules were inserted at 1400 h and removed at 2300 h. Groups of ovariectomized or sham-ovariectomized control animals had empty capsules implanted and removed at comparable times. Capsules producing basal E2 and P levels were not inserted after the removal of the original implant, since mean blood LH levels, pulse amplitude, and frequency were the same in rats sham ovariectomized or ovariectomized at 1830 h on proestrus and bled the next morning between 0930-1230 h. Mean blood LH levels decreased between the mornings of proestrus and estrus due to a reduction in LH pulse frequency as pulse amplitude remained stable. OVX at 0900-1000 h on proestrus increased mean blood LH levels 2.5-fold compared to values on estrus due to increases in both LH pulse frequency and amplitude. Restoration of physiological proestrous levels of only E2 returned LH pulse frequency to estrous values, but did not significantly affect LH pulse amplitude. P alone also had no significant effect on LH pulse amplitude, but slightly reduced pulse frequency, although, unlike E2, not to values seen on estrus. Replacing both E2 and P returned LH pulse amplitude to estrous levels and reduced LH pulse frequency.(ABSTRACT TRUNCATED AT 400 WORDS)

The object of this study was to determine the roles of ovarian estradiol (E2) and progesterone (P) in regulating pulsatile LH release between estrus and diestrous day 1 (D1) in the rat estrous cycle. Three groups of rats were bled at rates of 75 or 100 microliter whole blood/6 or 8 min, respectively, between 0930-1230 h on estrus or 24 h after either sham ovariectomy (OVX) on estrus (i.e. on D1) or OVX on estrus. There were no differences in plasma E2 and P levels in rats between estrus and early D1. However, after OVX on estrus, plasma levels of both steroids declined and were significantly lower 24 h later than values in D1 controls, indicating an active ovarian secretion of both hormones in this interval of the rat cycle. A significant increase in mean blood LH levels occurred between estrus and D1 due to an increase in LH pulse amplitude and frequency. After OVX on estrus, all parameters of pulsatile LH release also increased within 24 h, but mean blood LH levels as well as LH pulse amplitude and frequency were virtually identical to values in D1 controls, despite the decline in plasma E2 and P levels. Thus, OVX did not augment the increases in LH pulse amplitude and frequency that occur between estrus and D1. This demonstrates that the increase in pulsatile LH release from estrus to early D1 occurs in the absence of ovarian steroid negative feedback; the increases in LH pulse amplitude and frequency are not under negative feedback control by the low plasma levels of E2 and P present at this time. These data stand in direct contrast to the presence of prominent ovarian steroid negative feedback systems operative between D1 and diestrous day 2, and diestrous day 2 and proestrus.

Competitive binding assays using 125I-labeled equine LH confirm that this hormone binds with relatively high affinity to both LH- and FSH-binding sites on the separated Leydig cells and seminiferous tubules, respectively, of the 18-day-old rat testis. In contrast, ovine LH is potent only in Leydig cell LH-binding sites. However, despite its binding to FSH sites, equine LH, like all other LH preparations examined, lacks the ability to stimulate in vitro cAMP production from the rat seminiferous tubules, a characteristic action of FSH. Although all three species of LH examined (equine, ovine, and human) are similarly inactive in stimulating cAMP production when tested alone (all were

The object of this study was to determine whether the increase in LH pulse frequency and mean blood LH levels on day 22 of pregnancy in the rat is due to the precipitous fall in plasma progesterone (P) levels that occurs late in gestation. On day 20 of pregnancy two groups of animals with indwelling jugular cannulae were implanted sc with empty or P-containing Silastic capsules. Blood samples were withdrawn 0.5 h before and 5.5 h postimplantation on day 20 (0800 and 1400 h), at 1400 h on day 21, and at the end of the study between 1200-1300 h on day 22 to follow the time course of changes in plasma P levels over this 2-day period in both groups. These groups were bled on day 22 for 3 h between 0900-1200 h for analysis of pulsatile LH release. A third group not implanted with Silastic capsules was bled on day 20 for 3 h; plasma P levels in these rats bled on day 20 did not differ from the preimplantation values observed in either group of capsule-implanted rats. In empty capsule-implanted animals, plasma P values declined slightly from days 20 to 21 and were dramatically reduced between days 21 and 22. In contrast, after implantation of P capsules, plasma P levels were elevated on day 20 and remained elevated on day 21 compared with preimplantation values. Although these increased plasma P values declined between days 21 and 22, reflecting a decrease in endogenous P secretion, they were nonetheless comparable to day 20 values due to the presence of the P-containing capsules. Plasma estradiol values did not differ significantly between any of the experimental groups. In the empty capsule group bled on day 22, mean blood LH levels and LH pulse frequency were significantly higher compared to day 20 values, at a time when plasma P levels had fallen significantly from day 20 values. However, in the P capsule group, mean blood LH levels and LH pulse frequency on day 22 were significantly lower than values in the empty capsule group and were not different from the low values on day 20. Thus, preventing a decline in plasma P values to the low levels normally found on day 22 prevented the increase in LH pulse frequency and mean blood LH levels normally seen at this time of pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

The present studies were designed to characterize LH release during pregnancy in the rat. Unanesthetized animals with jugular cannulae were bled for 3 h between 1000-1300 h on days 6-8, 14-16 or 22 of gestation (50 microliters whole blood/5 min). Plasma estradiol and progesterone values both increased from days 6-8 to days 14-16. However, while plasma estradiol levels increased further between days 14-16 and day 22, plasma P levels had declined 86%. The percent coefficients of variation obtained for alterations in blood LH levels at each stage of pregnancy were all significantly greater than intraassay variation, indicating that LH release was pulsatile at each stage. Although there were no significant differences in mean blood LH levels, pulse amplitude, or frequency between days 6-8 and 14-16, the individual patterns of LH release clearly varied between these 2 groups, and most notably within the 14-16 day group. Fifty-three percent (9 of 17) of the LH records in rats on days 14-16 were nonpulsatile compared to only 20% (3 of 15) on days 6-8. However, despite a trend toward an absence of pulsatile LH release on days 14-16, mean frequency at this time did not differ from days 6-8, since on days 14-16 the remaining 8 animals demonstrated 3.5 pulses/3 h, while on days 6-8 the other 12 rats averaged only 2.5 pulses/3 h. On day 22, there was a marked increase in mean blood LH levels compared with either days 6-8 or 14-16. This increase was due to an increase in mean LH pulse frequency. All 15 rats demonstrated pulsatile LH secretion, a significantly greater incidence of pulsatile LH release than on days 14-16 (100% vs. 47%). These data demonstrate that LH release is pulsatile during pregnancy in the rat, and changes in the characteristics of this secretion occur at different stages of gestation.

The aim of this study was to determine whether the rapid increases in LH pulse amplitude and frequency that occur within 24 h after ovariectomy (ovx) on diestrus day 1 (D1) were due to the removal of progesterone (P) and/or estradiol (E). Initial studies demonstrated that plasma levels of E and P were 18.2 +/- 1.2 pg/ml and 34.1 +/- 3.2 ng/ml, respectively, between the evening of D1 and the morning of D2 in our colony of intact rats. Immediately after ovx and jugular venous cannulation on the morning of D1, rats were implanted either with empty Silastic capsules or capsules capable of restoring physiological levels of E and P to the control values reported above. These rats were continuously bled (75 microliter/6 min) for 3 h 1 day after ovx for analysis of pulsatile LH release, and then additional plasma samples were gathered for determination of E and P levels. Rats with empty capsules had decreased levels of E and P and increases in mean blood LH levels, LH pulse amplitude, and pulse frequency. Animals with E capsules had physiological levels of E and decreased levels of P, but no suppression of the acute post-ovx increase in pulsatile LH release. In contrast, animals with P capsules had physiological plasma levels of P, decreased levels of E, and a marked reduction in the acute LH response to ovx. This suppression was due entirely to a decrease in LH pulse amplitude, as pulse frequency was not altered. Rats with E and P capsules had physiological levels of these hormones, which resulted in an even greater reduction in the acute LH response to ovx. This suppression was due to decreases in both LH pulse amplitude and pulse frequency. The effect of P on LH pulse amplitude was centrally mediated, since the in vitro response to LHRH of anterior pituitary fragments from P-implanted rats was the same as that of anterior pituitary fragments taken from rats with empty capsules. These studies demonstrate that the acute increase in LH pulse amplitude that occurs within 24 h after ovx on D1 is due to the absence of a central inhibitory effect of ovarian P, while the rapid increase in LH pulse frequency is due to the loss of both ovarian E and P.(ABSTRACT TRUNCATED AT 400 WORDS)