Luteinizing Hormone Ovulation Research Articles

Changes in plasma progesterone, estradiol, follicle-stimulating hormone and luteinizing hormone during diestrus and ovulation in rats with 5-day estrous cycles: effect of antibody against progesterone.

Progesterone secretion remained significantly higher during diestrus in the 5-day cyclic rat than in the 4-day cyclic animal. Injection of a sufficient amount of antiprogesterone serum (APS) at 2300 h on metestrus in a 5-day cycle advances ovulation and completion of the cycle by 1 day in the majority of animals (75 and 80%, respectively). Progesterone (250 micrograms) administered with APS eliminated the effect of the antiserum. Within 2 h after administration of APS, levels of both follicle-stimulating hormone (FSH) and luteinizing hormone (LH) elevated significantly, while a significant elevation of plasma estradiol above the control value followed as late as 36 h after the treatment. None of the 5-day cyclic rats treated with APS showed ovulatory increases of FSH and LH at 1700 h on the second day of diestrus, although 3 of the 4 animals receiving the same treatment ovulated by 1100 h on the following day. The onset of ovulatory release of gonadotropins might have been delayed for several hours in these animals. These results indicate that recurrence of the 5-day cycle is due to an elevated progesterone secretion on the morning of diestrus, and suggest that a prolongation of luteal progesterone secretion in an estrous cycle suppresses gonadotropin secretion. Rather than directly blocking the estrogen triggering of ovulatory LH surge, the prolonged secretion of luteal progesterone may delay the estrogen secretion itself, which decreases the threshold of the neural and/or hypophyseal structures for ovulatory LH release.

Effect of FSH Treatment on LH and FSH Receptors in Chronic Cystic-Ovarian-Diseased Dairy Cows2

This experiment was conducted to 1) determine whether chronic cystic-ovarian-diseased (CCOD) cows fail to respond to luteinizing hormone (LH) treatment because of a lack of adequate ovarian LH receptors and 2) determine the effect of follicle stimulating hormone (FSH) treatment on ovarian LH and FSH receptors in ovaries of CCOD cows. The CCOD cows were those that did not resume cyclic ovarian activity after repeated treatment with human chorionic gonadotropin (hCG) and(or) LH-releasing hormone (LHRH) and were considered chronic by veterinarians. Thirteen CCOD cows were purchased from producers; six of them were injected with 5 mg FSH twice daily for 3 or 5 d (TCCOD) and the remaining seven remained untreated. Seven control (noncystic) cows in the luteal phase of the estrous cycle were injected with Lutalyse approximately 48 to 50 h before slaughter so they would be in the follicular phase (FP) of the cycle at the time of slaughter. Analysis of serum and pituitaries showed no differences (P greater than .05) in mean concentrations of serum or pituitary LH and FSH or pituitary LHRH receptor concentration and affinity among FP, CCOD and TCCOD cows. Ovarian follicle wall concentrations of receptors for LH (3.2 +/- .6; 13.0 +/- 2.5; 22.4 +/- 5.1 fmol/mg protein) and FSH (10 +/- 2.6; 43 +/- 7.2; 29 +/- 6.7 fmol/mg protein) were lower (P less than .05) in CCOD cows compared with FP and TCCOD cows, respectively. The same pattern was observed for concentrations of granulosa cell LH and FSH receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Modulation of ovarian LH receptor and serum hormone levels in rats with hyperprolactinemia induced by administration of ovine prolactin or sulpiride.

Hyperprolactinemia was experimentally produced in rats by administration of ovine prolactin (oPRL) and sulpiride, and tried to evaluate the effect of hyperprolactinemia on ovarian receptor for luteinizing hormone (LH) as well as that on serum gonadotropin and steroid hormone levels. Wistar-Imamichi strain mature female rats showing 4-day estrous cycles were treated with various doses of oPRL or sulpiride twice a day for 4 days from diestrus. They were killed on the fifth day. Binding of ovarian LH receptors was reduced by a small dose of oPRL (0.1 IU) or sulpiride (0.25 mg) and restored to normal by larger doses of oPRL. However, larger doses of sulpiride (50 or 100 mg) increased the receptor bindings beyond the control level (4.39 +/- 0.40 ng/mg homogenate protein). Serum prolactin levels decreased in rats treated with larger doses of oPRL, but increased with larger doses of sulpiride. Serum LH levels increased with both agents. Although the ovaries treated with either oPRL or sulpiride suggested the lack of ovulation, there were no significant changes of steroid hormones in oPRL groups. In contrast, sulpiride treatment resulted in a reduction of estradiol and an increase of progesterone secretion, suggesting the prolonged effect of the drug. Thus, prolactin appeared to act on the rat ovarian LH receptors in two different manners in hyperprolactinemia, depending on the amount of this hormone or a ratio of prolactin to LH.

Detection of the ovulatory luteinizing hormone (LH) surge with a semiquantitative urinary LH assay.

We examined blood concentrations of ovarian steroid hormones (E2, P) and serum LH concentrations to establish that the Ovu-STICK assay reliably reflects endocrine events in the periovulatory period. In all 16 cycles studied, which included 2 cycles in which the women received CC, the ovulatory surge of LH was detected with the use of the Ovu-STICK assay. In contrast, BBT monitoring correctly predicted the ovulatory event in only half the cycles.

Changes in ovarian luteinizing hormone and follicle-stimulating hormone receptor content and in gonadotropin-induced ornithine decarboxylase activity during prepubertal and pubertal development of the female rat.

Ovarian hCG and FSH receptor content was measured at different postnatal ages (days 4-32), at 4-day intervals, and expressed as counts per min 125I-labeled hormone bound/micrograms DNA. Specific FSH binding was minimal at day 4 and increased to a maximum at day 28, with the greatest rate of increase between day 4 and 16. hCG receptor content increased 6-fold between day 4 and 32, but contrasting with FSH, its greatest rate of increase occurred between day 16 and 28. The effectiveness of in vivo treatment with LH in inducing ovarian ornithine decarboxylase (ODC) activity, measured in 20,000 X g supernatants by the in vitro formation of 14CO2 from labeled ornithine, increased significantly during prepubertal development (days 21-33), paralleling the changes in hCG receptors. Ovarian hCG and FSH receptor content was also measured during the time of puberty. Specific hCG binding increased from anestrus (juvenile 32-day-old animals) to 1300 h of the first proestrus. The levels declined significantly by 1600 h of first proestrus and reached minimal values by the morning of estrus. Specific FSH binding also increased from anestrus to first proestrus, but to a much lesser degree, the levels showing only minor fluctuations during the rest of the cycle. hCG receptors measured in granulosa cells during puberty increased to an even greater extent than in the whole ovary; binding exhibited an 8-fold increase from anestrus to 1300 h of first proestrus and then declined to much lower values on estrus and the first diestrus. The capacity of LH to induce ovarian ODC activity increased markedly between anestrus and first proestrus, declining thereafter, and again paralleled the changes in LH receptor content. Evaluation of the kinetics of binding of hCG and FSH with their respective receptors in ovaries of 28-day-old rats revealed that the binding of hCG reached equilibrium within 4-8 h, whereas the binding of FSH attained equilibrium between 12-24 h. In both cases, however, the labeled hormones were clearly dissociable from their respective receptors by addition of an excess of unlabeled hormone. Moreover, although the ovarian receptor content of both hCG and FSH increased during prepubertal development, the equilibrium association constant of either hormone with its receptor remained unchanged. The results suggest that the infantile increase in FSH receptors may be induced by the high serum FSH levels present at that age and that, as shown by others in hypophysectomized rats, the subsequent increase in hCG receptors is, at least in part, an FSH-dependent phenomenon. The parallel changes in hCG receptors and LH-induced ODC activity during pre- and peripubertal development strongly suggest that an increase in LH binding capacity plays a fundamental role in the process of ovarian growth. It is also suggested that the changes in the steroidogenic ovarian response to hCG previously observed in peripubertal rats are, at least in part, determined by changes in ovarian LH receptor content.

Mechanism of the Postcoital Contraceptive Effect of Luteinizing Hormone-Releasing Hormone: Ovarian Luteinizing Hormone Receptor Interactions*

LHRH, via inducing inordinately high LH levels, can disrupt pregnancy in the rat. Based on studies indicating that LH can reduce gonadal content of its own receptor and thereby modify LH-dependent steroidogenesis, the effect of contragestational LHRH treatment on ovarian LH receptor dynamics was investigated. Pregnant rats were administered sc 200 ng LHRH/day during days 1–7 (pre- and periimplantation) or days 7–12 (postimplantation) of pregnancy. Vehicle-injected animals served as controls. At 1-day intervals, beginning the day after the first injection and continuing until the day after the final injection, animals were sacrificed for determination of pregnancy state, ovarian LH binding, and, in the postimplantational group, serum hormone levels. LHRH treatment resulted in a marked decrease in the number of normal implantation sites as observed by day 6 in the preand periimplantational groups and by day 11 in the postimplantational group. Ovarian LH binding in both LHRH treatment groups was significantly decreased within 24 h after a single injection and continued to be depressed throughout the course of treatment. The degree of LH binding to isolated luteal homogenates from postimplantational animals autopsied on day 9 after 2 days of LHRH or vehicle treatment suggests that the differences seen using ovarian homogenates reflect changes in luteal LH binding. Scatchard analyses indicate that the decreased binding is due to a lower LH receptor concentration (LHRH, 0.2–0.7 × 1015 M/mg wet wt; controls, 3.9–4.4 × 10-15 M/mg wet wt) rather than a change in receptor equilibrium constants (LHRH, Kd = 4.2–6.8 × 10-10 M; controls, Kd = 8.3- 10.0 × 1O-10 M). In both LHRH groups, the progressive failure of pregnancy and depression of LH binding were associated with decreased serum progesterone levels. The results from these experiments suggest that the mechanism by which LHRH terminates pregnancy involves a hypersecretion of LH which produces a decrease in ovarian LH receptor content (downregulation) resulting in a disruption of ovarian steroidogenesis, thereby removing gestational support. (Endocrinology 105: 139,1979)

Effect of electrochemical stimulation in the olfactory bulbs on the release of gonadotropin hormones in rats.

The olfactory bulbs were electrochemically stimulated in non-anesthetized, freely moving rats, and the ovulatory response and serum luteinizing hormone (LH) levels were studied. The stimulus was applied at 11:30 h through unilateral stainless steel electrodes chronically implanted, and serial blood samples were obtained by way of a plastic cannula located in the jugular vein. Electrochemical stimulation (100 microA/60 sec) of the main olfactory bulbs in the ventral aspect of the superficial layers as well as in its central core, performed on the day of proestrus, prevented the preovulatory discharge of LH and ovulation. Blockade of ovulation also occurred when the stimulus was applied in the lateral or medial parts of the superficial layers. On the other hand stimulation in the dorsal part blocked the preovulatory surge of LH and ovulation in only 50% of the cases. Stimulation applied in the accessory olfactory bulbs failed to interfere with ovulation and LH discharge. Stimulation of ovariectomized estrogen-primed rats applied in superficial layers of the main olfactory bulbs had no significant effect on the release of LH, but when the stimulus was applied in the accessory olfactory bulb a release of LH took place 3-6 h following stimulation. These results indicate that stimulation of the olfactory bulbs produce a dual effect on LH release: while the response of the accessory olfactory bulb is facilitatory in nature, that of the main olfactory bulbs is inhibitory.

Median raphe stimulation and sham procedures inhibit the LH surge.

Acute electrolytic stimulation of the median raphe (MR) nucleus (MR Stim) between 13:00 and 16:00 h on proestrus blocked ovulation in 10 of the 21 rats tested, whereas all sham-treated (MR Sham, no current) animals ovulated normally (n = 12). MR Stim at 16:00 h on proestrus in individual cannulated rats 'turned off' the luteinizing hormone (LH) surge in all animals tested. Unexpectedly, MR Sham treatment also abruptly inhibited the LH surge, although all animals ovulated. Manipulations associated with acute surgical procedures (puncture of the dura mater, ether anesthesia alone) were also found to inhibit the LH surge, with the magnitude of LH inhibition directly related to the severity of the operative procedures performed (p less than 0.025). The results suggest (1) that inhibition of ovulation following MR stimulation can be attributed to a response to stress qualitatively similar but more severe than that experienced by the MR sham group, and (2) that inhibitory inputs to the ovulatory LH release mechanism cannot be studied using acute surgical procedures.

Changes in salivary peroxidase and polymorphonuclear neutrophil leucocyte enzyme activities during the menstrual cycle.

An elevation in salivary peroxidase activity has been found about the time of ovulation in 14 menstrual cycles in a total of six women. This peak coincided with the ovulatory luteinizing hormone (LH) and oestrogen peak in the four cycles in which endocrine studies were performed. Rises in some polymorphonuclear neutrophil leucocyte enzymes were also seen around ovulation. The possible use of changes in salivary peroxidase as a method for detection of ovulation is discussed.

Gonadal luteinizing hormone receptors and adenylate cyclase: transfer of functional ovarian luteinizing hormone receptors to adrenal fasciculata cells.

Luteinized rat ovaries contain a high concentration of particulate luteinizing hormone (lutropin, LH) receptors and a small quantity of lipid-associated receptors that float in the 360,000 X g supernatant fraction of ovarian homogenates. During fractionation of Lubrol-solubilized LH receptors and adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] from the ovary and testis, LH receptors and adenylate cyclase were coincident on gel filtration, but could be resolved during ion-exchange chromatography of soluble ovarian preparations and were completely separated by lectin-affinity chromatography on Sepharose-concanavalin A. For further analysis of receptor-adenylate cyclase coupling, the lipid-rich fraction of ovarian luteal cells was used to transfer gonadal LH receptors to isolated adrenal fasciculata cells. The lipid vesicles obtained from ovarian homogenates by flotation at 360,000 X g contained 5--10% of the ovarian LH receptors and were devoid of adenylate cyclase activity. During incubation of lipid-associated receptors with dispersed rat fasciculata cells at 16 degrees C, progressive incorporation of LH binding sites into the adrenal cells was observed. When adrenal cells bearing heterotopic LH receptors were incubated with 1 nM human choriogonadotropin, cyclic AMP production was consistently stimulated, with an accompanying increase in corticosterone production. These results indicate that LH receptors exist as separate entities from adenylate cyclase in the gonadal cell membrane and can become functionally coupled to adenylate cyclase to evoke cyclic AMP production and steroidogenesis in the host adrenal cells to which they are transferred.

Inhibition of Ovarian Luteinizing Hormone (LH) and Follicle-Stimulating Hormone Receptor Levels With an LH-Releasing Hormone Agonist During the Estrous Cycle in the Rat

A single injection of the luteinizing hormone (LH)-releasing hormone (LHRH) agonist [D-Ala6,des-Gly-NH2(10)]LHRH ethylamide to female rats on diestrus I produced a marked reduction in ovarian LH/human chorionic gonadotropin (hCG) and follicle-stimulating hormone (FSH) receptor levels, uterine weight, and plasma progesterone levels measured 2 days later on expected proestrus. A maximal inhibitory effect was seen after a dose of only 40 ng of the peptide. No consistent effect of the LHRH analog was seen on ovarian prolactin receptors. When the analog was injected on day 7 of pregnancy, the inhibition of ovarian LH/hCG receptors was of shorter duration and was much less sensitive than that in nonpregnant animals. These data indicate that ovarian LH and FSH receptors levels are highly sensitive to changes in endogenous gonadotropin secretion and suggest that the gonadotropin surge occurring spontaneously on proestrus may play an important role in the regulation of ovarian gonadotropin receptors during the estrous cycle.

The Effect of Aspirin (Prostaglandin Synthetase Inhibitor) on Ovulaton

To investigate the effect of a prostaglandin synthetase inhibitor on ovulation the serum levels of luteinizing hormone (LH) and follicle stimulating hormone were determined daily throughout the menstrual cycles of 3 normal women with regular menses before and during treatment with aspirin. The aspirin was taken for 6 days before and 2 days after the expected ovulation day at a dose of 100 grains/day reduced by 5 grains/day until the lowest dose that gave tinnitus was reached. 2 of the women showed LH spikes at the expected time during aspirin treatment; the 3rd did not but showed a delayed preovulatory surge 10 days after discontinuation of aspirin. The admittedly small study suggests that aspirin does not consistently inhibit ovulatory LH in vivo even in unusually large doses. It also dims somewhat the outlook for reliable and safe contraceptive drugs that work by inhibiting prostaglandin.

Inhibitory Effect of a Luteinizing Hormone (LH)-Releasing Hormone Agonist on Rat Ovarian LH and Follicle-Stimulating Hormone Receptor Levels During Pregnancy

When injected at the daily dose of 100 microgram on days 7 through 12 of pregnancy, the luteinizing hormone (LH)-releasing hormone (LHRH) agonist [D-Ala6, des-Gly-NH2(10)] LHRH ethylamide led to complete suppression of pregnancy and a 45% to 60% decrease in plasma progesterone concentration. The antifertility effect of the LHRH analog was accompanied by an early and almost complete inhibition of ovarian LH/human chorionic gonadotropin and follicle-stimulating hormone receptor levels. These data suggest that the antifertility effects of LHRH agonists are mediated by down-regulation of ovarian gonadotropin receptors and decreased luteal function.

THE SEQUENCE OF HORMONAL CHANGES DURING PROSTAGLANDIN INDUCED LUTEOLYSIS OF THE SUPERLUTEINIZED RAT OVARY

ABSTRACT Immature female rats were pre-treated with pregnant mare's serum gonadotrophin (PMSG) and human chorionic gonadotrophin (HCG) to achieve superluteinization. Eight days after the HCG administration luteolysis was induced by sc injection of 5 μg of the prostaglandin F2α (PGF2α) analogue cloprostenol (Estrumate®). The serum levels of progesterone, 20α-dihydroprogesterone (20α-DHP), prolactin (PRL) and luteinizing hormone (LH) as well as the number of ovarian LH binding sites were measured during the first 23 h after cloprostenol injection. The serum levels of progesterone decreased from 500 to 200 ng/ml within 25 min after cloprostenol administration. A further decrease to 20 ng/ml occurred during the next 4 h, and serum progesterone remained low for the rest of the period. An increase in serum prolactin (PRL) to values between 28 and 44 ng/ml was observed after 3 h and the values remained elevated for the next 7 h. Although the serum levels of progesterone declined immediately, the serum 20α-dihydroprogesterone (20α-DHP) levels remained at 60 to 140 ng/ml for the first 5 h and then gradually increased to values corresponding to the initial progesterone levels 14 to 23 h after treatment. The number of ovarian LH binding sites was between 1.2 and 1.4 × 10−12 mol/mg protein during the first 9 h after prostaglandin (PG) injection, and then decrreased to 0.8 and 0.5 × 10−12 mol/mg protein at 14 and 23 h, respectively. The serum LH levels remained below the limit of detection for the assay (10 ng/ml) throughout the observation period. PGF2α injection induced the same basic changes in the serum levels of progesterone and 20α-DHP as cloprostenol treatment. Thus, the first effect of PG treatment measured was an immediate decline in the serum levels of progesterone, and this decline probably initiated the subsequent increase in pituitay PRL and ovarian 20α-DHP secretion. Therefore, the decrease in the number of ovarian LH binding sites appeared to be a consequence rather than a mediator of luteolytic effects of the prostaglandins.

Levels of Luteinizing Hormone (LH), Follicle-Stimulating Hormone, and 17β-Estradiol in Response to D-Trp6-LH-Releasing Hormone During Different Phases of the Menstrual Cycle in Normal Women

The response of serum LH, FSH, and 17beta-estradiol (17b-E) to stimulation with D-Tryp6-LH-releasing hormone (LH-RH analog) was measured in 34 normal women. The analog was administered either by vein, muscle, or continuous iv infusion in doses from 1 to 50 mcg during different phases of the menstrual cycle. The increase in LH and FSH to 10 mcg analog was significant (p .05) in all phases of the menstrual cycle by 60 minutes postadministration and lasted for at least 8 hours. 17b-E increased significantly by 8 hours. LH-RH analog was 40 and 21 times more potent than LH-RH in the stimulation of LH and FSH, respectively, during the follicular phase. In the ovulatory phase, LH and FSH responses differed kinetically from their responses in the other phases, and gonadotropin release was both faster and greater. The gonadotropin responses of 3 men when compared with those of the female subjects were almost always smaller (p .05). Because of the greater potency of this LH-RH analog, it may be useful in the treatment of infertility.

Hormonal and Clinical Responses in Amenorrheic Patients Treated with Gonadotropins and a Nasal form of Synthetic Gonadotropin-Releasing Hormone

Synthetic gonadotropin-releasing hormone (GnRH) in the form of nasal drops was self-administered by five amenorrheic patients in an attempt to assess its therapeutic value in anovulatory infertility. After follicular maturation had been induced with human menopausal gonadotropins (HMG), a total daily dose of 7.5 mg of GnRH in the form of nasal drops was self-administered at 2-hour intervals for 6 hours on 3 consecutive days. In four patients, plasma luteinizing hormone (LH) levels were significantly elevated over a period of at least 8 hours. In three of these patients, in addition, there was a definite upward shift in the basal body temperature (BBT) curve, and uterine bleeding occurred 6 to 9 days after the first dose of GnRH. In the fourth patient, ovulation was induced as indicated by a biphasic BBT curve, a plasma progesterone level of 13 ng/ml, and a luteal phase of 15 days. In the remaining patient, there was a borderline LH response and no clinical response. It is concluded that GnRH, in the form of nasal drops, is effective in eliciting and maintaining elevated plasma LH levels in patients in whom follicular maturation has been induced with HMG. By obtaining ovulatory LH levels, such a regimen can lead to ovulation. In addition, intranasal self-administration of GnRH is convenient and may provide an alternative route of administration for long-term therapy with this hormone.

Stimulatory feedback action of estradiol and estrone on LH release in the ovariectomized rat: roles different between limbic system and preoptic area.

Stimulatory feedback action of estradiol (E2) and estrone (E1) on luteinizing hormone (LH) in ovariectomized rats was investigated. A single dose of 20 mcg E2 (primed) caused a 24-hour periodicity of LH secretion that was low at noon and high in the evening. The 2nd dose of E2 given 72 hours later potentiated the LH secretion approximately 2 1/2-folds higher 30 hours after treatment. E1 injection markedly induced an LH increase in rats bearing medial preoptic area (MPO)-roof cut. Both estrogen derivative implants in the suprachiasmatic (POSC) and periventricular portions in the PO area evidently induced an increase of serum LH. The results suggest that the neuronal elements from which the transected fibers in the MPO-roof cut rats originated are the main positive feedback sites for E2 for the induction of the ovulatory LH discharge. Progesterone injection in E2-primed rats as well as progesterone implants in the POSC produced a marked increase in serum LH.

Characterization of an Inhibitor for Luteinizing Hormone Receptor Site Binding

An inhibitor for luteinizing hormone (LH) receptor site binding has been partially purified from aqueous extracts of ovaries from pseudo-pregnant or pregnant rats. The LH receptor binding inhibitor (LH-RBI) was heat-resistant, partially inactivated by trypsin or pronase digestion, and had a molecular weight of approximately 3800 daltons. The LH-RBI was not found in the ovary of mature non-pregnant rats or immature rats, nor was it found in testis or liver extracts. The LH-RBI strongly inhibited the in vitro binding of 125I-labeled ovine LH to ovarian LH receptors but did not inhibit 125I-labeled ovine prolactin binding to ovarian PRL receptors.

Effect of synthetic luteinizing hormone releasing hormone on ovulation during the oestrous cycle in the rat.

ABSTRACT The effect of synthetic luteinizing hormone releasing hormone (LH-RH) on ovulation has been studied during the oestrous cycle in adult female rats. Ovulation could be induced by the administration of 1 μg synthetic LH-RH at 1:00 a. m. on the day of dioestrus II (lights on from 10:00 p.m. to 10:00 a.m.). At 1:00 a.m. on the day of dioestrus II, the average volume of the largest follicles reached a volume of 83 × 106 μm3 and was three fifth of the volume of that at 6:00 a. m. on the day of pro-oestrus (critical period). These findings suggest that the luteinizing hormone (LH) content in the pituitary gland during the early period of dioestrus II is sufficient to induce ovulation and that the follicles that reach to three fifth of the volume at the critical period are capable of ovulating providing endogenous ovulatory LH released.

Coitus-induced ovulation

This article reviews evidence of coitus-induced ovulation. Maintenance of reproductive efficiency by more than 1 mechanism for triggering ovulation is interpreted as an evolutionary phenomenon aimed at ensuring the survival of the species. In earlier research estrogen levels or progesterone output were believed to regulate the ovulatory luteinizing hormone (LH) release and the length of the receptive period in spontaneous ovulators; more recently the effect of neural olfactory and emotional stimuli has been recognized. The neuroendocrine systems involved in spontaneous and reflex-induced ovulation include the hypothalamic-hypophyseal-gonadokinetic system and the neurohormonal pathways for coitomimetic stimuli. In spontaneously ovulating rodents the stimulus of coitus serves as an inducer for pseudopregnancy. The translation of vaginal stimulation into gonadomimetic humoral messages released from the hypothalamus and/or the posterior pituitary for the liberation of LH and prolactin is not completely understood. Nervous or biochemical influences resulting from coitus may even more directly affect ovarian functions by local sympathetic reflexes or by biochemical components of the ejaculate. In coitus-induced ovulation central nervous and/or peripheral autonomic nervous involvement may interact to push ovarian follicles toward maturation and ovulation or may help to ovulate nearly ripe or ripe follicles as a result of cohabitation. Acceptance of coitus-induced ovulation in humans renders rhythm methods of fertility control unreliable. In 1 large study of pregnancies resulting from rape 33-46% of conceptions occurred during what should have been a safe period. Emotions may also play a role in facilitating or predisposing to coitus-induced ovulation. There is a need for further biochemical statistical and demographic analyses of the frequency and sociologic importance of coitus-induced ovulation in humans.