Study Objectives
· To define amenorrhoea-oligomenorrhoea, dyspareunia, gynaecomastia, hypogonadism, impotence, infertility, menarche, menopause, menstruation and phases of the menstrual cycle, oligospermia-azoospermia, sterility, and virilization.
· To describe anticonception, anovulatory cycles, bleeding disturbances, castration, cryptorchism, postmenopausal hormonal alterations, puberty, anabolic steroids and doping, genetic and psychosocial sexual disorders.
· To explain the effect of anabolic steroids, the normal menstrual cycle, conception, implantation, pregnancy, pregnancy tests, birth and suckling. To explain the normal ovarian and testicular function, gametogenesis, erection, ejaculation and sexual satisfaction (orgasm). To explain the effect of androgen-binding protein, inhibin, aromatase, and the biosynthesis of steroids.
· To use the above concepts in problem solving and case histories.
Principles
· The gonads are concerned with the well being and preservation of the human race.
· The sperm decides the genetic sex (genotype). The Y chromosome is a constant determinant of maleness.
· Foetal differentiation of the genital ducts and of the external genitalia requires foetal gonadal hormones. The foetal genital tract will always develop into female genitals, if unexposed to embryonic testicular secretion.
Definitions
· Amenorrhoea-oligomenorrhoea are terms used for absence - irregular, infrequent menstrual periods. These signs suggest female hypogonadism, when pregnancy is excluded.
· Azoospermia describes absence lack of sperm in the ejaculate
· Dyspareunia refers to female pain or discomfort during intercourse.
· Gametogenesis is the formation of ova and sperm. The primitive germ cells are divided by meiosis, so the number of chromosomes is halved (22 autosomes and one sex chromosome).
· Genetic sex is determined by the presence or absence of the Y chromosome. The Y chromosome determines the development of testes and maleness. The Y chromosome contains a sex determining region (the SRY gene), which encode the testis determining factor (TDF).
· Genital sex is the phenotypic sex (apparent female or apparent male).
· Gonadal sex is determined by the presence of normal ovaries or testes.
· Gynaecomastia refers to the occurrence of female breasts in males. The causes are HCG-producing tumours, oestrogens or oestrogenic drugs.
· Hypogonadism (male) refers to a condition with small, soft testes producing little sperm and testosterone. The condition is usually found with subfertility.
· Impotence is inability of the male to produce an adequate erection for satisfactory sexual intercourse.
· Infertility (subfertility) is a diagnosis used on a couple, which has been unable to conceive during one year of unprotected intercourse. The causes are oligospermia, tubule blockage, ovulatory disorders, or combined problems with both persons in the couple.
· Menarche refers to the age at the first menstrual period.
· Menopause refers to cessation of periods, which usually occurs around the age of 50 years.
· Menstruation is the onset of spontaneous regular uterine bleeding.
· Oligospermia refers to reduced numbers of sperm in the ejaculate. The causes are primary testicular disease or blockage of the vas deferens.
· Puberty is the transition period from a non-reproductive to a reproductive state.
· Sterility refers to individual infertility. Chemotherapy and other drugs may cause sterility. Surgical blockage of the tuba or the vas deferens results in sterility.
· Virilization is the occurrence of male secondary sex characteristics in the female.
· Definitions of other genetic concepts are given in Chapter 31.
Essentials
This paragraph deals with 1. The sexual drive , 2. Sex before birth, 3. The menstrual cycle, 4. Ovulation/Female orgasm, 5. Conception, 6. Breast development, 7. Labour, 8. Efferent activity during coitus, 9. Sex hormones, and 10. Male puberty.
1. The sexual drive
We feel the sexual drive or desire for sex (libido), when sex-related areas in the higher brain centres are stimulated. These centres include the limbic system, Stria terminalis and the preoptic region of the hypothalamus. The desire for sex is increased by androgens in both sexes.
The sex desire of females is variable - for some it increases near the time of ovulation, when oestradiol secretion is increasing, while others experience a peak drive near menstruation. The CNS cells involved (see above) must contain sex hormone receptors. Sex hormones are steroids. They are lipid soluble and pass the cell membrane easily. After binding to cytoplasmic receptors (the steroid-thyroid family), the receptor-hormone complex translocates to the cell nucleus. Here the information is transcribed and translated. The result is release of new proteins with the same information into the cytosol, where the physiologic response is triggered. Castration is assumed to reduce female libido minimally, but male libido is most often lost. Removal of one testis need not change the male libido. These clinical observations reflect psychosocial differences, and not necessarily a different libido mechanism in the two sexes. Hypothyroid persons lose their sex drive. The sex desire (libido) is stimulated by a multitude of sense impressions (visual, auditive, olfactory, and psychological). Potency refers to the ability to engage in intercourse.
The brain is an important sex organ. Obviously, any natural body contact can be considered part of a healthy sex life - including the penetration of the penis in the vagina.
Sexual satisfaction is synonymous with orgasm in Western cultures. Orgasm is the psychological climax or the culmination of total commitment in a sexual act that is accompanied by a series of physiologic reactions. Female orgasm involves spinal cord reflexes similar to those involved in male ejaculation (see later). One very important reaction is ovulation, which is an automatic consequence of copulation among many animal species and periodically in humans.
Sexual enjoyment covers several phenomena. For example the fetishist satisfaction of wearing the clothes of the opposite sex. This is the important part of a transvestites sex life. Some transvestites become asexual in the general sense of the term, since they do not need partners. Some individuals prefer masturbation (onany) as a substitute for partnership. Many individuals prefer heterosexual contacts; others prefer homosexual activities, while bisexuals may prefer either sex - depending on the circumstances. Sexual activities can vary. Besides, homosexual activity, oral sex, anal sex and many other variants are not uncommon.
2. Sex before birth
Normal sexual development in the embryo involves several processes. The sperm, which can be an X or an Y chromosome sperm, decides the genetic sex or sex genotype (Fig. 29-1). The genetic sex is independent of the ovum.
If the ovum is fertilised by an X spermatozoa (22 + X-chromosomes) the offspring is XX, a female. If the ovum fertilises by an Y spermatozoa (22 + Y-chromosomes) the offspring is XY, a male (Fig. 29-1).
Fig. 29-1: The sperm decides the genetic sex. The presence of the Y chromosome is the determinant of maleness.
Sex differentiation in the embryo usually harmonises with the sex genotype, but hormonal disturbances can lead to abnormalities. Proliferation of non-germinal and germinal cells in the genital ridge creates the gonadal primordia, which develops into a cortex surrounding the medulla. Until the 7th week of gestation, each sex has a bipotential system (the sexual indifferent stage) with both Wolffian and Müllerian ducts. The urogenital sinus develops into the external genitals in both females and males.
Around the 7th week, the medulla of the primitive gonad begins to differentiate into a testis, if an Y chromosome is present. This is because the Y chromosome contains the so-called SRY gene (the sex determining region of Y), which encodes the testis-determining factor.
As the testes grow and their Leydig cells start to produce testosterone, the Wolffian ducts develop into the male reproductive tract (epididymis, vas deferens, seminal vesicles and the ejaculatory ducts), whereas the Müllerian ducts regress. Testosterone stimulates the growth and differentiation of the Wolffian ducts in the male. The regression of the Müllerian ducts is caused by the antimüllerian hormone from the Sertoli cells.
Conversely, in the female, the cortex of the indifferent gonads differentiate into ovaries, if only two X chromosomes are present and no Y. In the female foetus, where there is a developing ovary and no antimüllerian hormone, the Müllerian ducts develop into the female reproductive tract (the uterine tubes, uterus and the upper vagina), and the Wolffian ducts degenerate because the ovary does not secrete testosterone.- When a normal female foetus is exposed to androgens during the period of differentiation of the external genitalia, an apparent male can result.
Visible differentiation of the gross anatomy does not appear until late in the second month of embryonic life. Testosterone causes the differentiation of the foetus to a male. The foetal genital tract will always develop into female genitals, if unexposed to embryonic testicular secretion. The genital sex is a phenotypic female. If testosterone is present, male external sex organs develop and the genital tubercle elongates to form the male phallos. If testosterone is absent, female organs develop instead. It is the action of testosterone and 5-a-dihydrotestosterone on the urogenital sinus that is behind the normal development of the male external genitalia. In the last months of gestation the growth of the external genitalia depends upon foetal pituitary LH.
One population of cells in the indifferent gonade develops into the granulosa cells of the ovarian follicle and the Sertoli cells of the testicular seminiferous tubules. These cells support and mature the germ cells. – Another population of so-called interstitial cells develop into the theca cells of the ovary and the Leydig interstitial cells in the testis. The Leydig interstitial cells secrete testosterone, in response to human chorionic gonadotropin (hCG) from the placenta.
The presence of normal ovaries or testes determines the gonadal sex. Without normal ovaries or testes any genetic sex will develop into an apparent female.
Foetal plasma growth hormone (GH) concentrations are high, but GH-receptors are deficient and foetal GH is not essential for linear growth. Prolactin and placental GH act as growth factors and induce the presence of IGF-1 and IGF-2. A small transfer of maternal thyroid hormone is important for early foetal development. At birth, the babys own thyroid hormone is important for CNS development and somatic growth. Foetal PTH stimulates the Ca2+-transfer across the placenta and controls plasma-Ca2+. Foetal ACTH is important late during gestation in particular at birth, and the cortisol concentration is high in umbilical cord plasma. Foetal pancreatic a-and b-cells are functional by 14 weeks of gestation, but their release of glucagon and insulin is low.
In 1949 Barr et al. found a densely coloured body in the periphery of the nucleus (the Barr body or sex chromatin) of the buccal mucosa of females. The Barr body is also present in other individuals with two or more X-chromosomes in each cell. Individuals with one sex chromatin (Barr body) also have a drumstick attached to a small fraction of their leukocytes (Fig. 29-6). We find sex chromatin and drum sticks in cells, whether they divide or not. Chromosomes are only visible in dividing cells. The maximum number of sex chromatin and drumsticks is always one less than the number of X-chromosomes (Fig. 29-6).
3. The menstrual cycle
The menarche is the age at the first menstrual bleeding. It often occurs between the 12th and the 14th year.
LH and FSH are coordinators of gonadal function. The secretion of these pituitary gonadotropins is regulated through negative feedback by the plasma concentration of gonadal steroids. LH stimulates the interstitial cells of the ovaries (and testes), but LH also acts on female granulosa cells. LH binds to a LH-receptor, which spans the cell membrane several times. The LH receptor acts via adenylcyclase and with cAMP as a second messenger. Prostaglandins may increase the cAMP effects. Maintained stimulation by LH down-regulates the number of LH-receptors on the surface of gonadal cells.
FSH acts on ovarian granulosa cells (and testicular Sertoli cells) by binding to FSH-receptors, partially homologue with the LH-receptors. The increase in cAMP following FSH-receptor binding transcribes the aromatase gene and stimulates oestrogen synthesis. FSH stimulates synthesis of inhibin and peptide/protein products from granulosa and Sertoli cells. FSH amplifies the sensitivity to LH by increasing the number of LH-receptors on granulosa cells.
LH and FSH increase glucose oxidation, lactic acid production and protein synthesis.
The menstrual cycle starts at the first day of bleeding (menstruation). The bleeding is due to decrease of oestrogen and progesterone secretion. The FSH and LH secretion start to rise and stimulate the growth of several follicles ‑ in particular following the bleeding. One of these – the dominant follicle – select itself by outstripping the others and grow so fast that the follicle can protrude more than 10 mm from the surface of the ovary. The dominant follicle has an increased oestrogen synthesis due to increased aromatase activity. Oestrogen from the granulosa cells of the dominant follicle binds to specific, cytoplasmic receptors (of the steroid-thyroid-family) in the endometrial and other uterine cells. Oestradiol activates and stimulates formation of oestrogen and progesterone receptors.
Fig. 29-2: The menstrual cycle in a female.
Oestrogen increases the thickness of the endometrium, the size of the myometrial cells and the number of gap junctions thus allowing the myometrium to work as a unit. The oestrogen phase is also called the proliferative phase. The concentration of sex hormones in plasma is shown in Fig. 29-2. Oestrogens work synergistically with progesterone to release gonadotropins by positive feedback just before ovulation.
Following the rupture of the follicle (ovulation), the corpus luteum produces increasing amounts of progesterone in addition to oestradiol also from a new developing follicle (Fig. 29-2).
Due to the priming effect of oestrogen on progesterone receptors, both hormones stimulate the growth of the endometrial glands, so that they curl like a helix. The progesterone effect in particular provides the endometrial/myometrial tissues with their high secretion and bloodflow, so the uterus is prepared to receive the fertilised ovum. During sexual stimulation the vaginal fluid secretion increases, as does the bloodflow of the organs involved.
If fertilisation does not occur, the level of oestradiol and progesterone switches off both gonadotropins. The corpus luteum fades out and degenerates with no LH to support it (Fig. 29-2).
The ovarian hormones almost cease to flow, and the uterus is deprived of their stimulating action. Therefore the uterus shrinks and sheds its swollen lining.
On the first day of the menstrual bleeding, the low progesterone and high prostaglandin level probably releases enough Ca2+ to start spontaneous contractions of the myometrial cells. Ca2+ -ions enter myometrial cells and stimulate their activity in the secretory (progesterone) phase.
The gap junctions synchronise these contractions, so that they include the whole myometrium. This can make excretion of blood and necrotic cells (containing prostaglandins) extremely painful. Prostaglandins dominate in menstrual fluid and stimulate the spontaneous activity of the human myometrial cells. A normal bleeding corresponds to a loss of up to 50 ml of whole blood. The mixture of vaginal fluid and menstrual blood produces a pH close to that of normal blood. The average cycle length is 28 days.
ADH (vasopressin) secretion from the neurohypophysis can cause pre-menstrual tension and an unpleasant increase in body fluid volume.
4. Ovulation/Female orgasm
Ovulation
A sudden increase in the plasma level of oestradiol maintained for more than 24 hours can increase FSH output by positive feedback. This is called the positive feedback release ovulation. The pulsatile release of GnRH from the hypothalamus is possibly stimulated by the high oestradiol concentrations in mid-cycle and oestradiol increase the number of GnRH receptors on the gonadotropic cells of the anterior pituitary. A neural hypothalamic pulse generator has been proposed to be involved in ovulation, and in some cases female orgasm triggers ovulation.
At lower plasma levels oestradiol is a potent inhibitor of GnRH secretion and thus of FSH and LH output (negative feedback). The negative feedback forms the basis for the ovulation-inhibition by contraceptives.
LH binds to a membrane LH-receptor and acts via a G-protein, adenylyl cyclase and cAMP. LH mobilises cholesterol and its conversion to progesterone.
FSH acts on ovarian granulosa cells and testicular Sertoli cells by binding to a membrane receptor homologous with the LH-receptor. The binding increases the transcription of the aromatase gene, the oestrogen and the inhibin synthesis.
The primary inhibitor of FSH secretion is the peptide, inhibin, that is secreted by the ovary (and testis), and blocks the effect of GnRH.
The oestradiol release from the dominant follicle increases sharply in the last part of the follicular phase. This triggers the preovulatory surge of gonadotropins (LH and FSH).
The LH surge induces an enzyme that increases the synthesis of leukotrienes, prostaglandins and thromboxanes. These molecules create an inflammation that causes rupture of the follicle. LH continues to act on the follicular granulosa cells, turning them into a yellow endocrine organ, the corpus luteum.
Orgasm
The time for preplay including clitoral and multifocal stimulation is important for most females. A clitoral orgasm in the preplay often triggers more female orgasms later during the intercourse. Female orgasm is released from the spinal cord reflexes via sympathetic signals in the pudendal nerves.
Two persons with a simultaneous sexual drive must have the necessary time for the sexual act. If they are also in love, it is natural to explore and use all means to satisfy each other.
Years ago, when the Kinsey report was made, the average duration of sexual intercourse was measured in seconds in the US. American males able to ejaculate even faster were assumed to be particularly virile. Today, such a short performance is considered a male disease called premature ejaculation.
5. Conception and pregnancy
Conception
Approximately 100-200 million sperms are produced each day of the fertile lifespan. The female foetus may contain 6 million oocytes, but the number decreases throughout her life (less than half a million at puberty and she may have 500 ovulations before the menopause).
The autonomic moving spermatozoa passes through the uterus while prostaglandins inhibit their spontaneous activity. The spermatozoa can keep their vitality for more than 2 days, if they reach the fallopian tube. They lose their protective cover in the fallopian tube. The head of the spermatozoa swell and liberates proteolytic enzymes. These enzymes can dissolve the zona pellucida around the egg (oocyte). All these events in the spermatozoa takes days before it meets with the oocyte. The oocyte can only live 12-24 hours without conception.
Pregnancy
Many sperms bind to the zona pellucida, but only one penetrates the wall – and blocks the entry of other sperms. Fusion of the two sex cell membranes forms the zygote, and the mitosis is complete within 24 hours.
The zygote passes into the uterine tube within a few days, protected against other spermatozoa by an increased permeability for K+, so that the zygote membrane hyperpolarises. Peristaltic movements of the tube and ciliary motion conduct the zygote to the uterine cavity while undergoing cleavage division. Each cell is capable of developing into a complete human being up to the eight-cell stage.
At the morula stage, the cells start to develop into the inner cell mass or blastocyst, and the trophoectoderm or trophoblast. Seven days after conception, the blastocyst loses the zona pellucida and implants in the wall of the uterus (nidation). Nidation depends on prior conditioning of the endometrial stromal cells by progesterone bringing it into the proliferative phase. The stromal cells accumulate nutrients and swell or decidualize around the blastocyst. Endometrial laminin and fibronectin facilitate adhesion. Histamine and prostaglandins increase the permeability of the vessels around the nidation site. More than 2/3 of all conceptions result in miscarriage, because of insufficient attachment or other anomalies.
The foetal trophoblast, which give rise to the extra-embryonic tissues differentiates into two cell types. An inner layer of cytotrophoblasts, and an outer layer of syncytiotrophoblasts. The cytotrophoblasts synthesise stimulatory hormones such as CRH, GnRH, TRH and steroids.
The syncytiotrophoblasts synthesise first of all human chorionic gonadotropin (hCG). The b-group of hCG is specific and detected in maternal plasma 6 days following conception by specific antibody methods. The hCG is detectable in the urine within 9 days after conception.
The placenta is a fantastic hormone factory, which produces large amounts of hCG, relaxin. oestradiol, progesterone and human chorionic somatomammotropin (hCS or human placental lactogen, hPL). The hPL is synthesised from the 4. week of gestation. The hPL stimulates maternal lipolysis and inhibits insulin effects, causing hyperglycaemia.
The hCG is chemically related to TSH, FSH and LH. The hCG acts like LH and binds to the LH-receptors. The secretion of hCG is stimulated by GnRH produced by cytotrophoblasts. This is what keeps corpus luteum in being, and the pregnancy continues.
During pregnancy, hCG thus conserves the corpus luteum, taking over the role of LH.
The secretion of hCG stimulates ovarian release of progesterone and oestrogens just like LH. The hCG stimulates production of relaxin, inhibits the maternal secretion of LH and stimulates the maternal thyroid gland causing struma or hyperthyroidism in some pregnant females. Inhibin A from foetal trophoblasts peaks within the first week and suppresses maternal FSH secretion. Inhibin B concentrations remain low throughout gestation. LH and FSH concentrations in foetal plasma peak in mid gestation.
Fig. 29-3: Variations in plasma hormone concentrations during a normal pregnancy (42 weeks).
The plasma [hCG] reaches a peak value after 10 weeks of pregnancy, when the syncytiotrophoblast count is maximum (Fig. 29-3). - Shortly after delivery hCG disappears.
The first peak on the plasma progesterone curve is progesterone produced by corpus luteum. The placenta takes over the progesterone production during the remaining pregnancy period ending with a peak concentration before birth. Progesterone protects the foetus in the uterine cavity by stimulation of endometrial glands that nourish the zygote and by maintenance of the decidual cells. Progesterone inhibits uterine contractions (inhibits prostaglandin synthesis and oxytocin sensitivity).
The foetus and the placenta form a foetoplacental unit. It produces all the hormones necessary for a successful pregnancy. Steroid precursors are delivered from both the foetus and the mother. Oestrogen (oestradiol, oestrone, and oestriol) concentrations rise steadily throughout pregnancy (Fig. 29-3). Oestrogens stimulate the growth of the myometrium and of the ductal system of the breast. Oestriol production independs on the foetal adrenal cortex, so maternal plasma oestriol provides an estimate of the foetal condition.
The placental progesterone blocks the menstrual cycle of the mother. Pregnant females therefore develop amenorrhoea.
6. Breast development
During puberty FSH, LH, growth hormone, and insulin are important for the breast development. The thyroid hormones (T3/T4) are permissive. Before puberty, plasma LH and FSH concentrations are low. There is no reaction to the low concentrations of gonadal steroids and inhibin.
Oestrogens are growth factors for the myometrium and for the ductal system og the breast during pregnancy. At the end of pregnancy there are other hormonal events. Progesterone secretion reaches a peak and then falls. This fall in progesterone allows the pituitary to release prolactin (LTH).
Prolactin from the maternal pituitary rises throughout pregnancy. Prolactin acts on the enlarged mammary glands turning them into milk producers. Prolactin develops the milk producing acini in the breasts during pregnancy. Prolactin Inhibiting Factor (PIF or dopamine) from the brain inhibits the prolactin secretion.
The baby’s suckling stimulate the secretion of prolactin and oxytocin, but oestradiol and sexual stimulation is also involved. The mechanical stimulation of the breast increases the secretion of prolactin from the pituitary, but the response is strikingly reduced by alcohol.
Prolactin is important for the development of the mammary gland tissue, oxytocin, however, governs the ejection of milk during lactation. Oxytocin causes contraction of the myoepithelial cells in the milk ducts (just as it does in the myometrial cells).
Mother-milk contains long chain fatty acids that are essential for brain development. Suckling babies are protected against juvenile diabetes in comparison to non-suckling babies. Cow's milk contains much more protein and less lactose than human milk.
7. Labour
When the foetus has reached a critical size, the myometrial fibres are stretched, which increase their contractility.
At the end of pregnancy the uterus is sensitised by oestrogen. After a high peak in progesterone secretion the progesterone output falls. This fall in progesterone allows the uterus to respond to oxytocin, whose release is the final trigger for parturition.
The foetal pituitary-adrenal axis signals to the placenta a decrease in the progesterone-oestrogen ratio acting on the myometrium. This increases myometrial contractions that are mediated by prostaglandins (PGE2 and PGE2-a). A local increase in prostaglandin concentration increases myometrial cell Ca2+ and triggers uterine contractions. The density of oxytocin receptors in the myometrium increases throughout gestation and particular at term.
The role of the stable plasma concentration of maternal oxytocin at parturition is an enigma. Oxytocin is released according to a pulsatile pattern. The frequency of oxytocin pulsations increases at labour. This fact does not exclude an important role of oxytocin in normal human parturition.
Therapeutic doses of oxytocin initiate labour in most cases at the end of gestation,
The foetal cortisol production prepares the foetus to adapt to extrauterine life by stimulating lung maturation, by increasing the hepatic glycogen stores, and by promoting closure of the ductus arteriosus (Fig. 12-7).
Relaxin is an insulin-like polypeptide produced by the corpus luteum and placenta. The hormone relaxes pelvic articulations, suppresses myometrial contractions and softens the uterine cervix in order to facilitate passage of the foetus.
Several other factors are involved in human labour, but the exact trigger mechanism remains unclear.
8. Efferent activity during coitus
The activity in males is described as an example. The typical sequence of efferent events in the male includes erection, emission of semen and ejaculation.
Erection means penile rigidity and elongation due to parasympathetic vasodilatation. Psychological factors trigger penile rigidity, and sexual thoughts can cause erection, emission and ejaculation. The penis contains erectile tissue located in two dorsal corpora cavernosa and in a single ventral corpus spongiosum. All the cavernous spaces of the three penile corpora receive blood from thick-walled arteries ending centrally in each corpus. The blood leaves the cavernous spaces through thin-walled veins starting peripherally. Tactile stimuli, especially from the very sensitive glans penis activate sensory, somatic fibres in the pudendal nerve, whereby impulses reach the sacral plexus. Parasympathetic impulses (S2-S4) from the sacral plexus elicit dilatation of the arteries and constriction of the veins in penis. The cavernous spaces are hereby filled with blood under high (arterial) pressure within seconds, causing the penis to become hard and elongated for penetration. - Erection occurs quite normally during the REM phases of sleep.
Emission is caused by sympathetic contraction of smooth muscles (in epididymis, ducts and glands), which drive the fluids into the posterior urethra. Oxytocin ejects sperm into semen. Two exocrine glands near the neck of the bladder (the seminal vesicles and the prostate) secrete fluids that nourish the sperm and transport it through the urethra during the sexual act. The prostate gland supply an alkaline secretion containing Ca2+, Zn, and phosphatase to the ejaculate. The seminal vesicles supply fructose and prostaglandins. These two secretions neutralise the acid semen and help propel the spermatozoa towards the ovum. Seminal fluid also contains gonadotropins, sex hormones, inhibins, endorphins, relaxin, proteases and plasminogen activator. Epididymis supply sperm-coating proteins.
Ejaculation: Ejaculation is a sympathetic response. Contractions of skeletal muscles expel the semen from the urethra in a rhythmic pattern. Signals from glans penis reach the lumbar region of the spinal cord through afferent fibres in the internal pudendal nerves. Filling the posterior urethra with semen triggers sensory impulses that travel through the pudendal nerves to the spinal cord. The spinal cord transmits rhythmic signals to the skeletal ejaculation muscles (the ischio-and bulbo‑cavernous muscles and those of the pelvis). These rhythmic signals stimulate rhythmic contractions that expel the semen from the urethral meatus into the female genitals. – A typical ejaculate contains 300 million spermatozoa in 3 ml.
Inside the female genitalia the sperm is subject to the process of capacitation, which takes place within 6 hours. The sperm head is coated with substances from the ejaculate, Ca2+ enters the sperm, sperm motility increases, and the ability to penetrate the ovum is enhanced. The acrosomal membrane fuse with the outer sperm membrane, so that pores are formed and proteolytic enzymes can reach the surface of the sperm head.
9. Sex hormones
Sex hormones are oestrogens, progesterone, androgens and eichosanoids. Steroid synthesis in the gonads begins with cholesterol from acetyl Coenzyme A, and is almost identical to that of the adrenal cortex.
Oestrogens stimulate the female genitals and act to produce female secondary sex characteristics when a female enters puberty. Oestrogens and progesterone all enters the cell cytosol easily and bind to cytoplasmic receptors of the steroid-thyroid family. Oestradiol increases the synthesis of oestrogen- and progesterone-receptors.
These sex characteristics include the progressive growth of fallopian tubes, uterus, vagina, and external genitalia; also the fat deposition in breasts, buttocks, and thighs (Fig. 29-4). The ductal and stromal growth of the breasts is initiated just as the general growth at puberty with increased RNA and protein synthesis in the body cells. Oestrogens stimulate secretion of prolactin from the pituitary lactotrophic cells, increase the thickness of the endometrium and the size of the myometrial cell and their number of gap junctions. Oestrogens stimulate the hepatic production of essential proteins (eg, TBG, blood clotting factors, plasminogen, and HDL), but they inhibit formation of antithrombin III and LDL. Retention of salt and water can cause oedema.
Oestrogens consist of oestradiol, the principal ovarian oestrogen, oestriol, the major placental oestrogen, and oestrone, an important ovarian and postmenopausal hormone.
At a certain level oestradiol increases GnRH secretion and FSH output by positive feedback. There is also an increased LH sensi
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