Biomedical subjects

L S Frawley

Publications and source records attributed to L S Frawley.

At least 73 records · Page 4Linked to original sources

PubMed1991

Fluctuations in the proportions of growth hormone- and prolactin-secreting cells during the bovine estrous cycle.

Reverse hemolytic plaque assays were performed on monodispersed pituitary cells from cattle at various stages of the estrous cycle in an attempt to determine whether short term fluctuations in the gonadal steroid milieu influenced the proportions of pituitary cells that released GH and/or PRL. Phase of the estrous cycle was initially determined by gross ovarian morphology and later confirmed by determination of estradiol-17 beta and progesterone peripheral serum concentrations. Animals were subdivided into four groups according to phase of cycle: early luteal (EL; day 1-10), midluteal (ML; day 11-16), late luteal (LL; day 17-19), and follicular (F; day 20-21). Plaque assays demonstrated that the percentage of all pituitary cells that released PRL was greater in the EL phase than during the ML or F phases, whereas the relative abundance of GH-secreting cells remained unchanged. A more critical analysis of hormone-secreting subtypes revealed that the increase in total PRL secretors could be attributed almost exclusively to an increase in the abundance of those cells that released both GH and PRL (mammosomatotropes). Accompanying this augmentation of dual hormone-secretors was a decrease in the proportion of cells that released GH alone without a change in the abundance of cells that secreted only PRL. These results strongly suggest that during the estrous cycle there is a bidirectional interconversion among cells that release only GH and mammosomatotropes. Moreover, the relationship between ratios of acidophilic subpopulations and stage of reproductive cycle indicates that ovarian steroids may regulate this phenomenon.

Animals↗

PubMed1991

Stimulation of prolactin cell differentiation in vitro by a milk-borne peptide.

We have previously reported that the normal expression of PRL-secreting cells in neonatal rats requires a maternal signal specific to the first few days of lactation. These results raised the possibility that a milk-borne factor(s) ingested by the neonate and absorbed into the circulation might induce the ontogenic appearance of PRL cells. The purpose of the present study was to determine whether milk from this period could directly stimulate the differentiation of PRL secretors in culture. Monodispersed anterior pituitary cells from 1-day-old pups were cultured for 6 days with aqueous extracts of milk from early (days 2, 3, and 4) and late (days 15 and 16) lactation and then subjected to reverse hemolytic plaque assays for PRL and GH release. We found that the addition of milk extracts (10 mg/ml) from either early or late lactation stimulated the differentiation of PRL secretors (to 6.1 +/- 1.0% and 2.4 +/- 0.7% of all pituitary cells, respectively; mean +/- SE; n = 3) above that in control cultures without milk (0.2 +/- 0.2%). Thus, early milk was more than twice as effective as late milk in this regard (P less than 0.05). This effect appeared to be specific to PRL cell differentiation, since the relative abundance of GH secretors was not different between cells treated with either early or late milk (29.3 +/- 4.8% and 33.7 +/- 3.9%, respectively). On the other hand, late milk was more than twice as effective as early milk at increasing the capacity of GH secretors to release hormone (P less than 0.05). Preliminary characterization by gel filtration chromatography and proteolytic hydrolysis indicates that the bioactivity that differentiates PRL secretors is a small peptide(s) of 2000-6000 daltons. Taken together, our results demonstrate that a milk-borne peptide(s) is capable of specifically stimulating the differentiation of PRL-secreting cells in vitro, and that this bioactivity is more prevalent in milk from early lactation.

Animals↗

PubMed1991

Purification from human pregnancy serum of a low molecular weight mitogen similar to placental lactogen and growth hormone.

Recently, we isolated from the serum of pregnant women a factor that induced rapid proliferation of a lactogen-dependent rat lymphoma cell line (Nb2). This mitogenic factor is reasonably specific to pregnancy, since it was present in serum samples from second trimester as well as term-pregnant women, but not in those of adult men or cycling females. It is unlikely that this mitogenic activity (referred to as pregnancy mitogen [PM]) is due to contamination by classical lactogens, since acetone fractionation of serum yielded a preparation devoid of placental lactogen and prolactin, as determined by radioimmunoassays. Further purification of acetone precipitates from term-pregnant serum by ion exchange chromatography and gel filtration yielded a mitogenic activity with a relative mol wt of approximately 10,000. PM activity in the NB2 cell bioassay was not affected by the presence of prolactin antiserum. However, its activity was immunoneutralized by coincubation with anti-placental lactogen serum and, to a lesser extent, anti-growth hormone serum. It appears that PM was not generated by our extraction procedure, since gel filtration of whole serum also yielded a bioactive fraction of approximately 10 kDa. PM was further purified to homogeneity by high-performance liquid chromatography. Examination of the preliminary amino acid composition of PM revealed differences from that of a bioactive fragment of growth hormone and a corresponding portion of placental lactogen, suggesting that PM could be either a molecular variant of these hormones or a novel protein.

Amino Acids↗

PubMed1990

Suckling increases the proportions of mammotropes responsive to various prolactin-releasing stimuli.

It is well established that the suckling stimulus sensitizes or primes the anterior pituitary to PRL-releasing stimuli. It is also recognized that PRL-secreting cells from a given animal are not all alike but instead exhibit a considerable degree of functional heterogeneity. The goal of the present study was to determine whether the suckling-induced priming phenomenon is manifest at the cellular level by shifts in the relative abundance of various mammotrope subpopulations. This was accomplished by using reverse hemolytic plaque assays to evaluate the secretory characteristics of individual PRL secretors derived from lactating rats either before or after the transient application of a suckling stimulus. Groups of day 10 lactating rats separated from their litters for 4 h were either killed immediately or were reunited briefly (10 min) with their pups before death. Adenohypophyseal cells obtained after trypsin dispersion were then subjected to plaque assays for PRL. Mammotropes derived from suckled rats were, on average, considerably more responsive to the stimulatory actions of TRH and angiotensin II and less susceptible to inhibition by dopamine. Mammotropes from nonsuckled rats exhibited a bimodal frequency distribution in which plaques from the second mode were roughly 6-8 times larger (released considerably more PRL) than those from the first. Superimposition of suckling (or in vitro treatment with dopamine) caused the second mode to disappear. Suckling also enhanced greatly the fraction of PRL cells that shifted from the first to the second mode (i.e. released more hormone) after treatment with TRH or angiotensin II. Taken together, our results demonstrate that the suckling-induced sensitization of pituitary tissue to PRL-releasing stimuli is manifest at the cellular level as proportional shifts toward those cells most responsive to stimulatory secretagogues and away from those most susceptible to inhibition by dopamine.

Animals↗

PubMed1990

Bovine pituitary cells exhibit a unique form of somatotrope secretory heterogeneity.

Use of reverse hemolytic plaque assays revealed that, as in the rat, bovine somatotropes are functionally heterogeneous with respect to regulated GH release. Uniquely, this heterogeneity is manifested by the appearance of a distinct subpopulation of GH cells that release hormone only in the presence of the hypothalamic secretagogues GRF and/or TRH. Although these cells did not release GH in the absence of stimulatory agents, immunocytochemical detection of GH demonstrated these cells were capable of hormone storage. The relative abundance of silent somatotropes varied according to the hypothalamic secretagogue applied to the culture (GRF and/or TRH) and the physiologic state of the tissue donor. In cell cultures obtained from castrated males, 4.2 +/- 1.2%, 3.0 +/- 0.7%, and 6.8 +/- 1.2% (mean +/- SEM; n = 14) of all pituitary cells were induced to release detectable amounts of GH by GRF, TRH, and GRF/TRH, respectively. When pituitary cells obtained from gonad-intact males (n = 4) and females (n = 4) were tested, only incubation with GRF (14.1 +/- 2.5%; 6.9 +/- 2.3%, respectively) and GRF/TRH (15.2 +/- 2.4%; 9.2 +/- 2.6%, respectively) stimulated a significant population of these silent cells. A combined analysis of the proportion of GH secretors and the relative amount of hormone released per cell revealed that a substantial fraction of the GH secreted in vitro after stimulation is attributable to the recruitment of silent somatotropes into the secretory pool. Taken together, these results reveal the existence of a unique form of GH cell heterogeneity--the silent somatotrope. Moreover, our findings demonstrate that this somatotrope population could provide a cellular basis for the readily releasable pool of GH in the bovine pituitary.

Animals↗

PubMed1990

Is the mammosomatotrope a transitional cell for the functional interconversion of growth hormone- and prolactin-secreting cells? Suggestive evidence from virgin, gestating, and lactating rats.

Serum concentrations of PRL and GH increase and decrease, respectively, during the progression from nonpregnancy through lactation. However, it is unknown whether the secretory capacities and/or relative abundance of cells that release PRL or GH are altered during these physiological states. In the present study anterior pituitaries from adult virgin, gestating, and early or late lactating female rats were dispersed with trypsin and subsequently assayed for PRL and GH release using reverse hemolytic plaque assays. We found that the relative abundance of PRL-secreting cells was greater and that of GH cells lower in pituitaries from lactating females than in those from virgins. Moreover, the relative amounts of both PRL and GH released per cell were diminished in gestating and lactating females. For PRL, this decrease could be accounted for by an increase in the number of cells that released small quantities of hormone. We then performed simultaneous plaque assays to determine whether the shifts in the relative proportions of PRL and GH secretors were due to changes in the percentages of cells that secrete each hormone alone or in the fraction that releases both PRL and GH concurrently. Variations in both single and dual hormone-secreting cells appear to contribute to the overall fluctuations in the relative abundance of PRL and GH cells during these physiological transitions. We conclude that the additional PRL secretors present during lactation may arise from cells that previously released only GH, and that this functional interconversion of GH and PRL secretors might involve an intermediate cell type, the mammosomatotrope.

Animals↗

PubMed1989

Ontogeny of prolactin secretion in the neonatal rat is regulated posttranscriptionally.

PRL-secreting cells first appear in appreciable numbers on day 4 of neonatal life in rats. In the present study, we attempted to ascertain whether the ontogenic appearance of PRL mRNA and hormone release were temporally coordinated or discordant. Our results show that the PRL gene is expressed at least 3 days before the onset of secretion in newborn rats. Moreover, steady state levels of PRL mRNA in neonates are at least as high as those found in 10-day-old rats, in which 15-17% of all pituitary cells secret the hormone. This apparent blockage of translation is attributable to a lack of association of PRL message with ribosomes in the neonate. Taken together, these data indicate that the ontogeny of PRL secretion in rats is regulated translationally as well as transcriptionally.

Animals↗

PubMed1989

Relative importance of newly synthesized and stored hormone to basal secretion by growth hormone and prolactin cells.

It is generally accepted that under basal conditions there is preferential release of newly synthesized hormone by a number of endocrine cell type, including those that secrete GH or PRL. However, the cellular basis for this phenomenon along with the relative contribution of stored hormone to basal secretion has yet to be clearly established. In the present study, we employed reverse hemolytic plaque assays to monitor basal and stimulated release of GH and PRL from individual cells in which de novo protein synthesis had been blocked. Monodispersed pituitaries from adult male rats were cultured for 21 h in the absence or presence of maximally effective doses of puromycin (100 microM) or cycloheximide (36 microM) and were then subjected to separate plaque assays for GH or PRL. Treatment with puromycin reduced the percentage of GH or PRL secretors (plaque formers) by about half. Coincubation with stimulatory secretagogues did not increase the percentages of GH or PRL secretors in control cultures, but returned the proportion in puromycin-treated cells to normal, demonstrating that cells which failed to secrete basally could still release hormone from their stored pools when stimulated. Very similar results were obtained when these experiments were repeated with cycloheximide. Taken together, these results demonstrate that only a fraction of the cells that release GH or PRL are dependent upon newly synthesized hormone for basal secretion; the remainder appear capable of mobilizing stored hormone for this purpose even in the absence of stimulation.

Animals↗

PubMed1989

A cellular basis for growth hormone deficiency in the dwarf rat: analysis of growth hormone and prolactin release by reverse hemolytic plaque assay.

The purpose of this study was to elucidate the cellular basis for growth hormone deficiency in Lewis-derived dwarf rats. To this end, we used reverse hemolytic plaque assays to evaluate hormone release. This allowed us to determine the proportional abundance of GH- and PRL- secreting cells and estimate the relative amount of hormone secreted by individual pituitary cells from dwarf rats and their somatically normal counterparts. The percentage of all pituitary cells that released GH (formed plaques) in pituitary dispersions was substantially lower for dwarfs when compared with normals in the absence (3.8 +/- 2.2% vs. 43.4 +/- 2.2%) or presence (6.6 +/- 3.8% vs. 45.7 +/- 1.4%; n = 3) of GRF. In addition, GH secretors from dwarfs released less hormone (formed smaller plaques) than their normal counterparts under both basal and stimulated conditions. An analysis of the relative number of GH cells that formed plaques of various sizes was accomplished by constructing a frequency distribution. Dwarf GH secretors formed more small plaques and proportionately fewer larger plaques than normals under both basal and stimulated conditions. For comparison, we also quantified the proportions of PRL secretors and found that they were actually more abundant in dwarfs than normals in the absence (52.4 +/- 4.6% vs. 33.7 +/- 3.7%) or presence (53.4 +/- 4.9% vs. 33.8 +/- 4.1%; n = 4) of TRH. Treatment with this secretagogue consistently increased mean PRL-plaque area for both groups. Our findings demonstrate that dwarf rats are severely deficient in the proportion of GH secretors. In addition, the few GH secretors present in the dwarf pituitary were less responsive to GRF than normals. In contrast, PRL cells in dwarfs appear to be functionally similar to those of their normal counterparts. The reciprocal relationship in the proportions of GH and PRL secretors in dwarfs provides a rather unique model for investigating the functional relationship between these cell types.

Animals↗

PubMed1989

Pituitaries transplanted under the renal capsule contain functional growth hormone (GH) secretors and suppress GH and prolactin release from individual eutopic pituitary cells.

The extent to which pituitary explants secrete GH requires clarification. In the present study GH release from ectopic pituitary tissue was assessed using the reverse hemolytic plaque assay. In addition, the effects of this tissue on eutopic GH and PRL release were simultaneously investigated. Anterior pituitary glands from adult female donor rats were grafted beneath the kidney capsule of adult male hosts. Four weeks later, this ectopic pituitary tissue and the eutopic pituitary glands of the host animals were removed, dispersed with trypsin, and subsequently assayed for GH and PRL release. Contrary to expectations, we found that 37% of the ectopic pituitary cells were GH secretors. Furthermore, these GH cells remained highly responsive to GRF (10(-7) M), which evoked a 7-fold increase (P less than 0.05) in mean GH plaque area. By comparison, only 28% of these ectopic cells secreted PRL, and this release was not consistently augmented by exposure to TRH (10(-7) M). In the second half of this study we found that the presence of ectopic pituitary tissue severely compromised the secretory capacity of the eutopic pituitary cells. More specifically, GH-releasing factor induced a 3-fold increase in GH secretion from the eutopic pituitary cells of sham-operated control animals, but it enhanced the release from cells of host animals by only 2-fold. Moreover, the response to TRH by the eutopic PRL cells from explant-bearing animals was curtailed to such an extent that it was not significantly greater (P greater than 0.05) than basal release in that group. We conclude that the potential of pituitary explant cells to release GH is far greater than previously believed and that this ectopic hormone production may inhibit hormone release from the eutopic pituitary cells.

Animals↗

PubMed1988

Attenuation of growth hormone gene expression in desensitized somatotropes.

The effects of GRF-induced desensitization of somatotropes on GH gene expression were investigated on pituitary cells derived from male rats. Pretreatment of monodispersed cells for 18 hr with GRF abolished both the acute release of GH and the stimulation of GH gene expression in response to a subsequent 4 hr challenge with GRF. Concomitant preincubation with GRF and SS resulted in restoration of the ability of GRF to stimulate release of GH but not to augment GH gene expression. These results demonstrate that desensitization by GRF affects both the release of GH and GH gene expression, whereas the resensitizing effects of SS appear to be directed exclusively at the release mechanism.

Animals↗

PubMed1988

A cellular basis for functionally releasable pools in somatotropes.

In an attempt to define the cellular basis for the phenomenon of releasable pools, we compared the effects of two growth hormone (GH)-releasing peptides which differentially influence the dynamics of GH release. Monodispersed anterior pituitary cells from neonatal male rats were subjected to reverse hemolytic plaque assays for GH in the presence or absence of GH-releasing peptide (GHRP-6, an enkephalin-like hexapeptide) and rat GH-releasing factor (GRF). GRF increased the rate of plaque formation (an index of the rate of hormone release) from almost all somatotropes, whereas GHRP-6 influenced only half of these cells. Analysis of plaque sizes (which provides a relative index of the cumulative amount of hormone released per cell) revealed that GRF produced a bimodal frequency distribution of plaque sizes, demonstrating that some somatotropes released more hormone than others after treatment with a maximal dose of this secretagogue. This pattern contrasted with those of untreated and GHRP-6 treated somatotropes which each produced unimodal frequency distributions that were skewed to the left (toward smaller plaques) and were virtually superimposable at the end of a 4 h incubation. However, GHRP-6 greatly accelerated the rate at which the final size distribution pattern was attained. Taken together, these results suggest that GHRP-6 causes the immediate release of a limited pool of GH which is present only in a discrete subpopulation of somatotropes that respond to GRF. This pool may be identical to that which is released over a more prolonged period under basal conditions. Moreover, GRF appears to access a more substantial pool of hormone which is not released by GHRP-6. This pool is present in a small minority of somatotropes but probably accounts for a larger portion of the GH released by pituitaries stimulated with GRF.

Animals↗

PubMed1988

Liver tissue from lactating rats produces a factor that stimulates prolactin release and gene expression.

Liver tissue from nursing rats produces a substance, termed liver lactogenic factor (LLF), that potently stimulates casein release from isolated mammary cells. Inasmuch as the production of LLF is dependent on PRL, we decided to determine whether it could influence the release of the hormone by dissociated pituitary cells in culture. This was accomplished by measuring PRL release with a reverse hemolytic plaque assay and PRL gene expression with a DNA probe complementary to PRL mRNA. Treatment of pituitary cells from day 10 lactating rats with liver slice incubates from the same type of animal caused a 35.3 +/- 4.3% increase in PRL release during a 3-h incubation. Likewise, the same dose of LLF activity markedly increased (3.5-fold) the steady state levels of PRL mRNA. The responses were reasonably specific for PRL, since neither GH plaque development nor gene expression was affected by identical treatment. Taken together these results demonstrate that LLF can act directly at the pituitary level to exert positive feedback effects on both PRL release and gene expression.

Animals↗

PubMed1987

Hypothalamic factors differentially affect the proportions of cells that secrete growth hormone or prolactin.

Hypothalmic factors have been shown to regulate acutely the synthesis and release of adenohypophyseal hormones, yet few studies have investigated the long term effects of these agents on adenohypophyseal cell types. In the present study, we assessed the chronic influence of selected hypothalamic factors on the relative proportions of GH- and PRL-secreting cells in pituitary cultures derived from 5-day-old rats. Primary cultures were established and incubated for 6 days in the presence or absence of 0.1-microM doses of GH-releasing factor, LHRH, CRF, TRH, or vasoactive intestinal polypeptide and then subjected to reverse hemolytic plaque assays for analysis of the percentages of cells that released GH or PRL. In cultures from males, GH-releasing factor and LHRH treatment caused an increase in the proportion of PRL secretors and a commensurate decrease in the GH population. CRF increased PRL cells without affecting the GH secretors, while TRH reduced the percentages of both cell types, and vasoactive intestinal polypeptide had no effect. Virtually identical results were obtained for cells isolated from females. These results demonstrate that hypothalamic factors have the capacity to induce differential effects on the proportions of GH- and PRL-secreting cells. Surprisingly, our findings also show that hypothalamic factors that do not normally influence the acute release of GH or PRL can exert a chronic effect on the proportion of cells that secrete these hormones.

Animals↗

PubMed1987

Functional variations among prolactin cells from different pituitary regions.

Reverse hemolytic plaque assays were used to compare the responsiveness of cells from different pituitary regions to the modulatory effects of human pancreatic GH-releasing factor (GRF), TRH, and dopamine (DA). Tissues from the peripheral rim (outer zone) and the central region (inner zone) of adenohypophyses from day 10 lactating rats were dispersed with trypsin, and the cells were placed into culture. On the following day, these cells were subjected to GH plaque assays (conducted in the presence or absence of GRF) and PRL plaque assays (performed with or without TRH and DA). Cells from both zones responded similarly to GRF with a rapid acceleration of GH plaque formation. However, the rate of PRL plaque formation in response to TRH and DA differed between cells from these regions. For outer zone cells, plaque development increased greatly with TRH treatment, but was only moderately affected by DA. Plaque formation from inner zone cells was influenced slightly by TRH, but markedly inhibited by DA. These results suggest that PRL, but not GH, cells from these pituitary regions are differentially responsive to at least two hypothalamic secretagogues. We then performed fixed sequential plaque assays to determine whether the proportions of cells that released PRL only (classical mammotropes) or those that released both GH and PRL (mammosomatotropes) also differed between the inner and outer zones. Using this approach, we found that the outer zone contained a much larger proportion of dual hormone secretors than did the inner zone. These results, when taken together with the responsiveness differences discussed above, raise the possibility that the release of PRL from mammotropes and mammosomatotropes is regulated differently and that the ratio of these two cell types may dictate, in part, the manner in which a specific region of the pituitary responds to hypothalamic input.

Animals↗

PubMed1987

Liver tissue produces a potent lactogen that partially mimics the actions of prolactin.

An in vitro bioassay (based on the detection of casein release from isolated mammary cells by reverse hemolytic plaque assay) was used to detect a lactogenic factor secreted by liver tissue from suckled rats. This material stimulates casein release in the absence of added PRL and is actually more potent than PRL in this regard. The substance(s) possesses the following additional characteristics: it is released from liver tissue of lactating but not virgin female or male rats; when tested together with PRL, its effects are additive rather than synergistic; and unlike PRL, it does not increase the proportion of mammary cells committed to casein release. These findings are consistent with the possibility that a Liver Lactogenic Factor may mediate, at least in part, the lactogenic component of PRL's action. This functional relationship may be similar to that which exists between GH and the somatomedins.

Animals↗

PubMed1987

Existence of somatotrope subpopulations which are differentially responsive to insulin-like growth factor I and somatostatin.

It is generally accepted that hypothalamic somatostatin and hepatic insulin-like growth factor I (IGF-I)/somatomedin-C act directly on the pituitary to inhibit GH release, but it is not known whether all somatotropes are responsive to these agents. In the present study, we used a reverse hemolytic plaque assay to compare the acute (8 h) effects of somatostatin and IGF-I on the release of GH from individual cells in 24-h cultures of male rat pituitaries. Treatment with these factors caused comparable dose-dependent decreases in both the rate of plaque formation and the percentage of cells which released GH. In 8-h incubations, maximal (10(-8) M) doses of IGF-I or somatostatin alone decreased the percentage of GH-releasing cells to approximately the same degree (from 34.4% in controls to 29.7% and 28.4%, respectively), yet the effects of these factors were additive when both agents were applied to the same cells (to 24.5%). When we analyzed the sizes of plaques (an index of the amount of hormone released per cell) which resulted from these treatments, we noted that somatostatin was a much greater suppressor (to 11% of control value) of GH release than IGF-I (60% of controls). Coincubation with 10(-8) M GH-releasing factor had no effect on the percentage of GH-releasing cells at 8 h but completely overrode the inhibitory effect of IGF-I on plaque size without affecting the somatostatin-induced decrease in this regard. Taken together, these data suggest that IGF-I and somatostatin act, at least in part, on separate subpopulations of rat somatotropes. Somatostatin is a much more effective inhibitor of total GH release than IGF-I and appears to affect most, if not all, somatotropes. In contrast, IGF-I acutely inhibits GH release (prevents plaque formation) from some somatotropes, but does not seem to affect the remaining GH cells.

Animals↗

PubMed1987

Analysis of relaxin release from cultured porcine luteal cells by reverse hemolytic plaque assay: influence of gestational age and prostaglandin F2 alpha.

Relaxin release from dispersed luteal cells was detected by a reverse hemolytic plaque assay to determine the influence of gestational age on basal relaxin secretion. Monodispersed luteal cells were derived by collagenase treatment of corpora lutea obtained from pigs in early (days 19-26), mid-(days 47-62), and late (days 80-99) gestation. The rate of plaque development under nonstimulated conditions progressively accelerated as gestation advanced, as did the rate of increase in plaque size. These results unequivocally demonstrate that basal relaxin release increases with advancing gestation. However, only about 50% of large luteal cells released relaxin at all stages of pregnancy examined up to day 100. These data indicated not only that basal relaxin release increases during pregnancy, but also that considerable heterogeneity exists with respect to relaxin output by individual cells. In contrast, both the basal rate of relaxin release and the percentage of cells committed to relaxin release declined significantly when luteal cells derived from preparturient sows (days 107-112 of gestation) were examined. Exposure of cultured luteal cells to prostaglandin F2 alpha (10(-8) and 10(-6) M) resulted in a rapid stimulation of relaxin secretion, but this agent did not recruit additional cells into the secretory pool. These data are consistent with the idea that autonomous changes and the action of secretagogues may combine at different times to achieve overall regulation of relaxin release by the corpus luteum. The significance of nonrelaxin-releasing luteal cells remains to be determined.

Animals↗