Male sexual hormones

Sertoli cells of testis produce testosterone, Leidig’s cells – inhibine and estrogens.

Inhibine

• encourages feed-back connection with hypophysis which inhibits follitropine secretion

Testosterone

• determines sexual differentiation in ontogenesis;

• regulates sexual behavior (sexual attraction and libido);

• determines sexual signs development on male type: secondary male features – hairiness on face, in fossae auxillaris, genitals growth;

• performs spermatogenesis regulation;

• causes anabolic effect (to skeleton and body musculature) – growth stimulation;

• lack N, P, K and Ca in organism;

• activates RNA synthesis;

• stimulates erythropiesis.

FEMALE SEXUAL HORMONES:

• determines secondary female features development;

• determines female genitals growth and maturation;

• stimulates skeleton growth and maturation;

• encourages subcutaneous fatty cellulose accumulation by female type;

• control menstrual cycle.

Estrogens functions:

• inhibit folliculo-stimulating and luteinizing hormone secretion as well as decrease adenohypophysis answer to gonadoliberine action;

• possess anabolic action;

• enforce bone tissue metabolism and accelerate skeleton bones maturation (stop bone tissue growth at puberty coming);

• encourage Na and water lack in organism up to oedemas development (in big doses);

• influence on lipids exchange, decrease cholesterol level in blood;

• trigger sexual differentiation during ontogenesis;

• determine sexual maturation, female sexual features development, menstrual cycle formation;

• detect uterus muscle (myometrium) and epithelium (perimetrium) growth as well as stimulate proliferative (second) phase of menstrual cycle;

• regulate sexual behavior (by female type);

• increase uterus contraction and its sensitivity to oxitocine;

• regulate milky glands development;

• give weak anabolic effect;

• increase osteoblasts activity.

Progesterone functions:

it is estrogens antagonist; so, it limits their proliferative action in endometrium, myometrium and vaginal epithelium as well as causes endometrium changings necessary for fertilized egg cell implantation; thus, it preserves pregnancy;

it decreases uterus readiness to contraction;

activates endometrium secretory structures;

activates milky glands growth and development;

decreases gonadotropins secretion inhibiting by hypophysis;

encourages ovulation inhibiting during pregnancy;

possesses weak catabolic action;

causes antialdesteronic effect – Na-uresis.

Placenta hormones:

steroid:

• estriol;

• estron;

• estradiole;

• progesterone;

peptide:

• gonadotropine or chorionic gonadotropine;

• somatomammotropine;

• thyreotropine;

• corticotropine;

• beta-endorphine;

• alpha-melanothropine;

• beta-lipothropine;

neuropeptides:

• thyroliberine;

• somatostatine;

• corticoliberine;

• gonadoliberine;

• somatoliberine.

Stress, general adaptation syndrome.

Stress – is a state of non-specific adaptative mechanisms tension occurring at excessive (superliminal) factors action to organism. Clinical manifestation is complex of structural, functional and biochemical changings receiving the name “general adaptational syndrome”. The term “stress” was described first and introduced in usage by Hans Selie in 1936.