We report the effects of sublingual absorption of a single dose (0.5 mg) of oestradiol-17 beta (E2) in 8 post-menopausal women, on plasma E2 and oestrone (E1), urine elimination of total E2 + E1 and on plasma FSH and LH. The results show that sublingual absorption of E2 occurs and that plasma concentrations of E2 obtained (between 133.2 to 320 pmol/l) in this way were higher than those obtained after percutaneous absorption of a single dose (3 mg) of E2. The ratio E1/E2 in plasma is close to that of pre-menopausal women.

Peripheral plasma from four postmenopausal women was analysed for oestrone (E1) and oestradiol (E2) during 48 hours after oral intake of a single tablet of 2 mg Progynon (oestradiol valerianate). Plasma levels of E1, E2 and d-norgestrel were analysed daily in five postmenopausal women during treatment with tablet Cyclabil (oestradiol valerianate in a biphasic preparation with dl-norgestrel) in 21 dyas. Radioimmunoassay (RIA) was utilized for the quantifications. Pretreatment plasma levels of E1 were about 20 pg/ml and E2 about 12 pg/ml. It is concluded that oestradiol valerianate is rapidly absorbed from the gastrointestinal tract and converted to E1. This is reflected by plasma levels of E1 considerably higher than those of E2. The E2 levels found were in the range of those in ovulatory women, while the oestrone levels were higher.

Crystalline oestradiol-17 beta is poorly absorbed from the gastrointestinal tract. Three different fractions and a standard fraction containing oestradiol- 17 beta of a known particle size and surface area, were administered orally, to postmenopausal women, to test if changes in particle size will influence the absorption. The bioavailability of each fraction was determined by measurements of peripheral plasma oestrogens. Two different dosages of the standard fraction were given vaginally to compare the bioavailability after oral and vaginal administration. The gastrointestinal absorption was dependent of the particle size of oestradiol. The smaller particle the more rapid and effective absorption as reflected by increasing area under the plasma concentration curve of oestrone and oestradiol. The smallest particle, however, resulted in a pronounced initial oestradiol peak. The coarser particles were more slowly absorbed with more even plasma oestrogen elevation for a sustained period of time. The vaginal absorption of oestradiol was more effective than the gastrointestinal. When the same amount of an equal preparation according to particle size, was given vaginally the maximal plasma concentration was almost 40 times higher than when given orally.

The formation of [3H]oestradiol macromolecule complexes was studied in vivo and in vitro in the kidney, lung and liver of intact foetal guinea pig. Specific binding of [3H]oestradiol was demonstrated in the cytosol and nuclear fractions of foetal kidney. Intensive binding was found in the cytosol of foetal lung but most of the bound radioactive material (70 %) was [3H]oestrone. Some binding was found in the cytosol of foetal liver but not in the nucleus of this tissue. In the in vivo experiments, the binding of radioactive material to plasma proteins was studied: 22 % of the plasma radioactivity was bound of which 67 % was identified as oestrone sulphate. Oestradiol sulphate represented 7% and unconjugated oestradiol only 0.6 % (0.1 % of the total plasma radioactivity). On the other hand, 2-3 % of the foetal plasma radioactivity was found as unbound [3H]oestradiol. In the kidney, the formation of [3H]oestradiol complexes in the cytosol fraction does not depend on temperature while nuclear [3H]oestradiol complexes increase with increasing temperature. Maximal formation of [3H]oestradiol complexes in the cytosol fraction and the 0.1 M TRIS and 0.3 M NaCl nuclear extracts was reached after 15 min but binding in the 1 M NaCl nuclear extract continued to increase up to 30 min. After incubation of purified nuclei of foetal kidney with 1.1 x 10(-7) M [3H]oestradiol, specific binding was found in the different nucelar fractions. Specific binding was also detected in isolated nuclei previously extracted by 0.1 M TRIS and 0.3 M NaCl before being incubated with 1.1 x 10(-7) M [3H]oestradiol. The Kd of binding of [3H]oestradiol in the renal cytosol fraction is 2.5 x 10(-10) M with n = 4.5 x 10(-14) moles/mg protein. Incubation of isolated 1 M NaCl nuclear extract from foetal kidney with [3H]oestradiol gives a Kd of 3.3 x 10(-10) M with n = 2.5 x 10(-14) moles/mg protein. It is concluded that the nuclear complexes in the foetal kidney could be formed either through an intermediate cytosol complex or that the "two step" mechanism could take place in the nucleus. Furthermore, direct binding of [3H]oestradiol with high affinity was observed in the 1 M NaCl nuclear extract.

OBJECTIVE

To compare oestradiol and oestrone concentrations and bioavailability after a single dose and at a steady state during oral oestradiol valerate, transdermal oestradiol gel and transdermal oestradiol patch treatments.

METHODS

Two open, randomised, cross-over studies were conducted. In the first study, 12 healthy postmenopausal women received 1.5 mg oestradiol as a transdermal gel or a 2 mg oestradiol valerate tablet daily for 14 days. In the second study, 15 postmenopausal women were treated for 18 days with 1.5 mg oestradiol gel or a transdermal patch releasing oestradiol 50 microg/24 h (replaced every 72 h). Venous blood samples for serum oestradiol and oestrone measurements with RIA were taken until 24 or 72 h after the first and last doses.

RESULTS

The tablet and the transdermal gel yielded similar serum oestradiol profiles with a peak concentration 4-5 h after administration. The patch resulted in relatively stable oestradiol levels during the mid third of the wearing time whereas much lower levels were observed in the beginning and towards the end. There was no difference in the fluctuation between the peak and trough oestradiol levels between the gel (56 or 67%) and the tablet (54%) while the fluctuation was greater with the patch (89%). The bioavailability of oestradiol from the gel was 61% as compared with the tablet and 109% as compared with the patch. The gel was not bioequivalent with the tablet or the patch.

CONCLUSIONS

The doses used of the transdermal gel and the patch roughly corresponded to each other with regard to the amount of oestradiol absorbed whereas the bioavailability from the tablet was significantly higher than from the gel. The lack of bioequivalence, the different serum oestradiol profiles and the large intersubject variability suggest that individual dose adjustments may be needed when changing administration form.

Single milk samples collected during pregnancy from 128 Sahiwal (zebu), 295 Karan Swiss and 198 Karan Fries cows and 164 Murrah buffaloes were analysed for oestrone sulphate by a sensitive, direct, radioimmunoassay procedure developed in the laboratory. Mean oestrone sulphate levels were below detection limit (< 50 pg/ml) during the first 2 months of pregnancy in all animals. There was an exponential increase in the hormone concentration beginning at the fourth month of pregnancy in cows, although the rate of increase was greatest among Sahiwal cows, followed by Karan Swiss and Karan Fries cows in that order (P < 0.01). An exponential increase in oestrone sulphate levels was also recorded in buffaloes beginning at the fourth month of gestation. However, the mean hormone levels in this species, after initially being lower than Sahiwal and Karan Swiss cows up to 6 months of pregnancy, increased to higher levels thereafter. From this study it was concluded that in addition to genetic factors, environmental adaptation could also influence the oestrone sulphate levels. In addition, the study also provided a basis for pregnancy confirmation by milk oestrone sulphate determination after 110 days in gestation in cattle and buffaloes using a simple, direct, assay procedure.

Serum oestrone sulphate concentration was measured in samples taken from 1275 sows of four breeds or crossbreeds (large white, landrace, large white cross landrace and monarch hybrid) during the period 25 to 30 days after mating. A simple, direct radioimmunoassay using 20 microliter serum was employed for the estimation of oestrone sulphate and pregnancy diagnoses were made on the basis that more than 0.5 ng oestrone sulphate/ml serum indicated a pregnant sow and less than 0.5 ng/ml indicated non-pregnancy. Overall accuracy of pregnancy diagnosis based on oestrone sulphate was 98 per cent; this was not influenced by breed or day sampled (within the range tested). For pregnant sows, there was a positive correlation between serum oestrone sulphate level and litter size, although individual values could not be used to predict litter size for particular sows. Oestrone sulphate concentration was also measured in samples taken from pregnant monarch sows during the last third of the gestation period and the level was more than 0.5 ng/ml in 99 per cent of samples taken on day 77 or later. Thus, measurement of serum oestrone sulphate level in samples taken more than 76 days after mating could be used as a confirmatory test of pregnancy.

Single blood samples from 106 pregnant and seven non-pregnant Karan Swiss cows and 104 pregnant and nine non-pregnant Murrah buffaloes were measured for oestrone and oestrone sulphate hormones by radioimmunoassay. Mean plasma oestrone level was below detection limit (less than 2.5 pg/ml) in non-pregnant and 1 month pregnant cows and buffaloes. In cows the mean oestrone level fluctuated narrowly between 10.25 and 26.65 pg/ml between the second and eight months of pregnancy, followed by a steep rise in the ninth and especially in the tenth month (151.24 pg/ml). In buffaloes mean oestrone concentrations were lower and fluctuated between 14.81 and 23.56 pg/ml during the second to ninth months of pregnancy, rising sharply in the tenth month to a peak of 47.37 pg/ml. Mean oestrone sulphate levels were below detection limit (less than 16 pg/ml) during non-pregnancy, first and second months of pregnancy in cows, increasing sharply thereafter to a peak of 6401.38 pg/ml in the tenth month of pregnancy. In buffaloes, low mean levels of oestrone sulphate were recorded in the non-pregnant and up to the fourth month of pregnancy with the levels rising sharply thereafter to a peak of 6559.82 pg/ml in the tenth month. The hormone levels were not significantly different in the two species (P greater than 0.01). The possibility of using oestrone sulphate measurement as a test of pregnancy confirmation has been indicated for both species.

Detectable concentrations of oestrone sulphate were present in 50% of the plasma samples collected from pregnant animals by Day 17. No oestrone sulphate was detected in plasma from cyclic nonpregnant pigs.

The plasma concentrations of oestrone (Oe1), oestradiol (Oe2) and oestrone sulphate (Oe1S) were measured in the femoral artery (FA), femoral vein (FV) and hepatic vein (HV) in seven men and three postmenopausal women undergoing catheterization for the evaluation of cardiac arrhythmias. None of the persons had congestive heart failure; conventional liver function tests were normal, and they were without any medication. The plasma concentration (mean +/- SD) for Oe1 was 34.6 +/- 19.5 pM in HV, 134 +/- 71.6 pM in FV and 93.4 +/- 48.5 pM in FA. The plasma concentration of Oe2 was 29.9 +/- 19.7 pM in HV, 80.3 +/- 42.7 pM in FV and 55.2 +/- 28.1 pM in FA. The results support the concept of peripheral formation of Oe1 and Oe2 and hepatic removal. The plasma concentration of Oe1S was 980 +/- 469 pM in HV, 945 +/- 463 pM in FV and 937 +/- 461 pM in FA. The small difference in plasma level of Oe1S between FA and FV was insignificant. In all persons the plasma level of Oe1S was higher in HV than in FA and FV (2P less than 0.01) indicating a net formation of Oe1S in the splanchnic area.

The aim of the present study was to investigate the effect on blood coagulation and fibrinolysis of a natural oestrogen preparation, piperazine oestrone sulphate, prospectively in menopausal women. Scopolamine was given to the control group. The women were investigated before and during treatment with regard to factors VIII, VII, X, V, fibrinopeptide A, antithrombin III, plasminogen, rapid antiplasmin and alpha 1-antitrypsin. There was no significant change towards hypercoagulability or decreased fibrinolysis in any group. In the oestrogen group, however, a tendency towards an increased level of plasminogen and a decreased level of antiplasmin was demonstrated. In the scopolamine group there was an unexpected fall in factors X and V and also in plasminogen and alpha 1-antitrypsin. A low level of some blood coagulation factors in some of the women before treatment is somewhat astonishing; none of them had any history of excessive bleeding.

In breast cyst fluid obtained from 50 patients age (47.1 +/- 2.3) sodium, potassium, oestrone (E1), oestradiol (E2) androgens, progesterone, (P) and Epidermal Growth Factor--EGF were determined. Markedly higher oestrogens, progesterone, testosterone, and EGF-levels were detected in cyst fluid than in blood. These data have confirmed previous results and have clearly shown that breast cyst fluid with high potassium (ratio K/Na>> 1.0) contains more oestrogens, progesterone, testosterone, androstenedione and EGF than the group with low electrolyte ratio. This finding might be put in correlation with the fact that patients with high ratio K/Na may a higher risk of breast cancer than those with low electrolyte ratio.

Natural killer (NK) cells have been described as being very sensitive to oxidative stress. Thus it has been previously shown that chronic administration of oestrone in drinking water of athymic mice xenografted with a wide variety of human tumours, increases their growth and development. In this study an investigation was made to see whether oestrone supplementation could influence the NK cell activity by changes in the antioxidant defences which result in an oxidative stress and influence the proliferation of tumours. Supplementary oestrone was administered in drinking water of athymic mice xenografted with two different human tumours which lack oestrogen receptors: a bladder carcinoma and a small-cell lung carcinoma. The growth of the urothelial carcinoma was poorly affected by oestrone, but oestrone significantly (p<0.01) increased the proliferation of the small-cell lung carcinoma. The average uterus weight was increased by 62% in oestrone treated mice with no modifications in plasma zinc and selenium status, nor in erythrocyte copper zinc superoxide dismutase level. Nevertheless a slight decrease in erythrocyte glutathione peroxidase activity was noted. Trace elements and antioxidant enzymes in liver homogenates remained unchanged. Oestrone treatment also had no effect on plasma and liver lipid peroxides. The immune response was evaluated by measuring NK activity of splenocytes against 51Cr labelled YAC-I target cells. A 35.5% decrease in the NK activity (p<0.001) was observed after oestrone treatment and may be responsible for graft tolerance. However, the results of these experiments seem to exclude the role of oxidative stress in the modulation of NK activity.

The tritium water release assay, originally described for the analysis of aromatase activity in placental tissue, was used to estimate aromatase activity in breast tissue samples. The lower activity in this tissue necessitates longer incubation times and thus optimization of the assay conditions. To prevent oxidative and proteolytic inactivation of aromatase, dithiothreitol and albumin were added to the incubation mixture. Extra NADPH, cofactor in the aromatase reaction, also improved reaction rate in placental incubations, but after approximately 120 min activity rapidly decreased. Inhibitors gradually produced during the incubation could explain this phenomenon. Quantitative gas chromatography-mass spectrometry (GC-MS) analyses of testosterone, oestradiol, oestrone and androstenedione after incubation with non-labelled androstenedione proved that a substantial amount of the substrate is converted into testosterone. Qualitative GC-MS steroid profiling of the incubation mixture demonstrated the presence of hydroxylated oestradiol and hydroxylated testosterone, produced during incubation, which could have caused partial aromatase inhibition. The adjusted assay was used to analyse 84 breast tissue samples, histologically classified as normal, adenoma or carcinoma. Aromatase activity was found in 56% of all samples and ranged from 0.6 to 26 pmol oestrogen/g protein per hour. Aromatase positivity was found in 80% of the normal samples, 56% of the adenoma samples and 48% of the carcinoma samples. Although carcinoma samples were less often aromatase positive than normal tissue samples (chi2 = 4.80; P < 0.050) there was no difference in absolute aromatase activity. Because no less than approximately 50% of the carcinomas contained aromatase activity and because of the non-routine character of the assay we conclude that it is justified to start aromatase inhibition therapy without previous knowledge of the aromatase status.

The formation of oestrone sulphate has been examined in MCF-7 (oestrogen receptor positive, ER+) and MDA-MB-231 (ER negative, ER-) breast cancer cells. Using intact cell monolayers and a physiological substrate concentration, progesterone (1 microM) and dexamethasone (1 microM) both increased oestrone sulphate formation in MCF-7 cells. In MDA-MB-231 cells, dexamethasone, but not progesterone, increased conjugate formation. A number of growth factors, cytokines and human serum albumin (HSA), which have previously been found to regulate oestrogen synthesis, were also examined for their ability to regulate oestrone sulphate formation. In MCF-7 cells epidermal growth factor, acidic and basic fibroblast growth factors, insulin-like growth factor-type I and insulin all stimulated oestrone sulphate formation. The cytokines, tumour necrosis factor alpha (TNFalpha) and interleukin-1beta also increased conjugate formation in the ER+ cells, as did HSA. In contrast, in MDA-MB-231 cells TNFalpha was without effect and HSA inhibited oestrone sulphate formation. The ability to modulate oestrone sulphate formation in ER+ cells may be an important mechanism to limit the availability of oestrogen to interact with the ER.

OBJECTIVE

We evaluated the significance of single serum LH estimates (as assessed by radiometric assay (IRMA) and Leydig cell in-vitro bioassay (BIO)) for the diagnosis of polycystic ovary syndrome (PCOS) in women with infertility and cycle abnormalities.

METHODS

Hormonal and clinical comparisons between subgroups were made based on classification according to (a) rigid clinical and endocrine (excluding LH) characteristics of PCOS, (b) elevated IRMA-LH concentrations, (c) BIO-LH levels. In addition, androgen modulation of LH biopotency was studied in these patients.

METHODS

Ninety-nine women presenting at our infertility Unit with oligo/amenorrhoea.

RESULTS

Of the total study group, 35 women were diagnosed positive as PCOS and 42 showed elevated IRMA-LH levels. Only 51% (n = 18) of PCOS patients showed elevated IRMA-LH levels, and in PCOS significantly higher levels of BIO-LH, androstenedione, oestrone, and BIO/IRMA-LH ratios were found as compared to non-PCOS patients. In the group with elevated IRMA-LH only 43% (n = 18) of subjects were diagnosed as PCOS, and no difference in BIO/IRMA-LH ratios was found. With increasing BIO-LH levels the probability of PCOS rises sharply (P < 0.001), whereas this probability is of only marginal significance (P < 0.06) for IRMA-LH. In the total study group a correlation is observed between serum testosterone (T) levels and IRMA-LH (r = 0.47), and BIO-LH (r = 0.51) concentrations. This correlation is absent comparing serum T and BIO/IRMA-LH ratios (r = 0.15).

CONCLUSIONS

Results presented in this study indicate that (1) women with infertility and oligo/amenorrhoea classified based on signs of PCOS or IRMA-LH levels, exhibit different clinical and endocrine characteristics, (2) only 51% of PCOS women exhibit elevated IRMA-LH concentrations, and only 43% of women with elevated IRMA-LH were diagnosed as PCOS, (3) IRMA-LH levels are a poor predictor of PCOS, whereas the predictive value of BIO-LH is better, (4) elevated BIO/IRMA-LH ratios in PCOS are dependent on alterations in BIO-LH, rather than IRMA-LH concentrations, and (5) no correlation was observed between serum T levels and BIO/IRMA-LH ratios.

This study was designed to evaluate the long-term effect (6 months) of the luteinizing hormone-releasing hormone (LH-RH) agonist buserelin on pituitary and ovarian function in a group of 14 patients presenting with the polycystic ovarian (PCO) syndrome. Buserelin was given subcutaneously 200 micrograms three times daily for the first 7 days followed by 500 micrograms once daily. Blood samples were taken weekly for the first month and then every month for radioimmunoassay of LH, FSH and sex steroids. While LH levels were stimulated during the first 2 weeks and then declined towards baseline, serum FSH levels were reduced after only 1 week (P less than 0.05). Serum oestradiol levels were maximally suppressed to the menopausal range after 1 month and testosterone levels were also significantly inhibited (P less than 0.05) after 2 weeks of therapy. Dehydroepiandrosterone (DHEA) sulphate did not show any significant change while 17-hydroxyprogesterone was suppressed after the first month of buserelin administration (P less than 0.01). The apparent divergent response of the gonadotrophins and the reduction of ovarian steroids in spite of lack of suppression of LH levels can be explained by the marked inhibition of the bioactivity of LH assessed by dispersed mouse Leydig cells assay. The clinical evaluation of hirsutism did not detect any change during the 6 month period. No patient had any menstrual bleeding or spotting after the sixth week of buserelin. The monthly incidence of hot flushes varied between 50 to 66%. This study shows that LH-RH agonist administration can selectively inhibit ovarian function and could be an interesting approach to evaluate the respective contribution of the ovary and adrenal on the pathophysiology of the polycystic ovarian disease. Polycystic ovarian (PCO) syndrome is characterized by tonic and exaggerated secretion of LH leading to an excessive stimulation of the ovarian stroma and an increased production of androgens (Yen et al., 1970; DeVane et al., 1975; Rebar et al., 1976). The androgen precursor delta 4 androstenedione is transformed in peripheral tissues into oestrone (Siiteri & MacDonald, 1973), thus maintaining the state of pituitary hypersensitivity and creating a positive feedback (Yen et al., 1976). The starting point of this vicious circle is still controversial; some argue for a hypothalamic abnormality (Vaitukaitis, 1983) while others support the peripheral origin of the hypersecretion of steroids (Reyniak, 1983). The importance of the adrenal contribution in this syndrome is still unclear.(ABSTRACT TRUNCATED AT 400 WORDS)

The patient, diagnosed as a case of testicular feminisation in infancy, was examined at the age of 15 years because of severe symptoms of virilising puberty with poor breast development. Plasma steroid analyses revealed a 10-fold elevated androstenedione concentration (A: 1562 ng/100 ml). Testosterone (T: 266 ng/100 ml) was in the male pubertal range. Thus the A/T-ratio was far above normal. The oestrone/oestradiol ratio was also elevated (Oe1/Oe2: 10.2/2.2 ng/100 ml). A, T, Oe1 and Oe2 could not be suppressed by dexamethasone, but reacted promptly to fluoxymesterone (A: 781 ng/100 ml). hCG caused a further increase of the A/T-radio (2220/246 ng/100 ml); ACTH did not alter the A-concentration. These findings together with simular investigations after gonadectomy suggest that the failure to convert A to T and Oe1 to Oe2 is essentially located in the testes. In vitro incubations of testicular tissue showed reduced 17-ketosteroid reductase activity in tissue slices and in the subcellular fractions microsomes and cytosole. This form of male pseudohermaphroditism can easily be detected already in infancy, if steroid analyses and stimulation tests are performed. In case of female sex assignment patients should be submitted to early orchidectomy in order to avoid virilisation in puberty.

BACKGROUND

Alzheimer's disease is 1.5 to 3 times more frequent in women than in men. This fact can be biased as women as a group have more long life survival. Semantic memory and naming are more frequently and severely impaired in women.

METHODS

Both genetic and environmental factors can contribute when one determined case develops Alzheimer's disease. A known risk factor for this development in women is oestrogen deprivation in menopause: accumulated evidence does exist. After menopause, plasmatic levels of two main oestrogens, oestradiol and oestrone, fall. It has been suggested that this estrogenic deprivation would increase the risk of development of Alzheimer's disease in women. Conversely, estrogenic replacement could decrease that risk. There are several neurotransmitters whose systems were influenced by estrogens. Amongst them, there are included acetylcholine, serotonin and norepinephrine. Estrogenic replacement could ameliorate the brain function or also delay the development of Alzheimer's dementia syndrome, by acting over a number of metabolic targets. Prospectively, some action on certain groups of women at risk must be analyzed. Neuropsychological testing ad hoc will be evaluated, both for the patients with clinical disease and for the population at risk, in this late case to ascertain a possible delay in the appearance of Alzheimer's disease symptoms.

Urinary oestrone-3-glucuronide, oestradiol-3-glucuronide, oestrone and oestradiol were measured by radioimmunoassay methods adapted for the very low levels found in postmenopausal women. Oestrogen concentrations related to creatinine in morning urine samples from ten postmenopausal women were found to correlate well with total oestrogen excreted in 24 h (r = 0.934, 0.867, 0.947, 0.909, respectively; p less than 0.002). Day to day variation in five individuals, measured over 5 weeks, showed random fluctuations, with no obvious cyclical variation. Reference ranges, based on two consecutive morning urine samples from 131 postmenopausal women, were 0.73-4.57 mumol/mol creatinine for oestrone-3-glucuronide, 0.66-3.00 mumol/mol creatinine for oestradiol-3-glucuronide, 4.8-30.9 nmol/mol creatinine for oestrone and 3.8-16.8 nmol/mol creatinine for oestradiol. We suggest that such assays may have a part to play in the screening for women at greatest risk of developing osteoporotic fractures.

Two experiments were carried out to monitor influences on the uterine electromyographic activity (EMG) in cyclic gilts with chronic uterine EMG electrodes. In Exp. 1 the EMG was recorded continuously from Day -1 for 24 days and was evaluated for frequency, duration and amplitude. Progesterone and oestradiol in peripheral plasma were measured daily. As high amounts of oestrogens are characteristic for boar semen, in Exp. 2 the influence of seminal oestrogens on uterine contractions at Day 0 (first day of standing reflex) was investigated in gilts with chronic intrauterine catheters. They were infused with 10 ml saline (N = 4) or saline with physiological amounts of oestrogens (5 micrograms oestradiol + 2 micrograms oestrone + 4.5 micrograms oestrone sulphate; N = 4). Sham-treated gilts (infusion catheters, no infusion; N = 5) served as controls. The EMG was recorded for 2 h before and 9 h after infusion. In Exp. 1 the maximal amplitude (2040 +/- 98 microV) and duration (32 +/- 1.7 sec) but the lowest frequency (15.8 +/- 2.1 contractions/h) were found on Day 0. With decreasing oestrogen and increasing progesterone concentrations the frequency increased continuously until Day 5 (63.5 +/- 1.0 contractions/h) while the amplitude (183 +/- 13 microV) and duration (3.3 +/- 0.7 sec) decreased. During Days 6-13 the EMG activity was not detectable. The reverse pattern was found from the onset of luteolysis until the following Day 0. On Day 0 a significant correlation between oestradiol and the duration (r = 0.81; P less than 0.01; n = 10) but not the frequency was observed.(ABSTRACT TRUNCATED AT 250 WORDS)