Anterior pituitaries (APs) from lactating rats were studied in vitro to determine the mechanisms by which LH release, but not FSH release, is suppressed. Hemipituitaries were exposed for 4 h to GnRH (20 nM) or elevated potassium (K+; 57 mM) according to two different regimens: 6 min/h (pulsatile) or 60 min/h (continuous). Pulsatile K+ exposure stimulated similar amounts of LH release by APs from diestrous females and lactating females on day 5 or 10 who were nursing two or eight pups. Pulsatile GnRH stimulation resulted in significantly greater amounts of LH release from all groups than was observed after pulsatile K+, except by APs from females nursing eight pups. In this group, GnRH was no more effective than K+ in stimulating LH release by APs from day 5 of lactation, but was slightly but significantly more effective on APs from day 10 of lactation. The degree of suppression of GnRH-stimulated LH release was directly correlated with the intensity of the suckling stimulus, and removal of the eight-pup suckling stimulus for 48 h completely restored the LH response to GnRH to the response observed by APs from females on diestrous day 2. Exposure of the APs continuously to either K+ or GnRH produced results that were similar to those observed after the pulsatile regimen, except that the total amount of LH released during the 4-h incubation was greater. However, APs from females suckling eight pups still released significantly less LH in response to GnRH than did APs from females suckling two pups or diestrous females. FSH secretion by the APs was similar in response to either pulsatile K+ or GnRH stimulation and was not suppressed by suckling of a large litter. The total amount of FSH released by pituitaries from lactating and cycling animals did not differ significantly, except that by APs females deprived of their eightpup litters for 48 h, in which case pulsatile GnRH stimulated a greater amount of FSH release. However, the pattern of FSH release varied, in that pulsatile GnRH stimulation of diestrous pituitaries showed a priming response, whereas no priming response was evident during lactation. Exposure of APs to elevated K+ continuously produced little more FSH release than exposure to pulsatile K+ stimulation. However, continuous stimulation by GnRH generally released more FSH than did K+. FSH responses to GnRH by pituitaries from lactating females were similar or greater than the FSH responses by pituitaries from diestrous females. Significant priming effects of GnRH on FSH release were observed by pituitaries from diestrous animals and from day 10 lactating females who were nursing two or zero pups. However, no priming effects were observed by pituitaries from females suckling eight pups. The differences in LH and FSH responses to K+ or GnRH stimulation lend further support to the hypothesis that the mechanisms controlling LH and FSH secretion are not similar. The release of LH and FSH in response to K+, which may reflect release from a readily releasable pool, is generally not suppressed by lactation. The suppression of LH appears to be due to inadequate GnRH stimulation of the secretory processes that act to increase the amount of LH available for release. The similarity in FSH responses after pulsatile GnRH or K+ stimulation suggests that FSH secretion may be less dependent on the specific effects of GnRH to maintain normal basal secretion.
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