By

H.Khorrami Ph.D. http://khorrami1962.spaces.live.com

khorrami4@yahoo.com

EPA(Eicosa Pentaenoic Acid)

DHA( Docosa Hexaenoic Acid)

Polyunsaturated FA

PL-A2

PGE2 →+GnRH →+LH

Indomethacin in follicular phase → block ovulation

Catecholamines →+PGE2 →+GnRH

Estrogen →+PGE2 →+ LH

PGE2 stimulate GnRH in response to catecholamines

PGE2 stimulate LH in response to estrogen

So indomethacin blocks ovulation

LH →+cAMP →+PGF2α , PGE2 in follicles

PGF2α as luteolysis factor Cyclooxygenase inhibitor → prolong corpus luteum life

PGF2α → uncoupling of LH receptor from cAMP ( in minutes) → decrease steroidogenesis / loss of LH receptor ( in hours)

Progesterone secretion stimulated by PGE2 & inhibited by PGF2α

Adenosin ( a purine) amplificate LH action

The balance of adenosin/ PGF2α is important for luteal lifespan

LH stimulates PGF2α & PGE2

PGF2α is a luteolysin factor In minutes uncoupling LH receptor from cAMP

In hours loss of LH receptor

PGE2 stimulate progesterone secretion by granulosa cells

PGF2α inhibit progesterone secretion by granulosa cells

PGE2 inhibits spontaneous contraction

PGF2α stimulate tubular contraction (isthmic region)

Progesterone enhance PGE2 effect

PGF2α receptor predominantly in isthmic region

PGE receptor predominantly in ampulatory region

PGF2α stimulate tubular contractility

PGE2 inhibit spontaneous contraction Enhanced by progesterone

Infertile & took contraceptive …. contraction in response to PGE2

Gravid uterus…. contraction in response to PGE2 & PGF2α

Non-gravid. . . .diminished response

Response depends on various stages

Nonpregnant generally is stimulated by PGE2 & PGF2α

lower sensitivity at the time of ovulation

PGE2 → uterine contraction(in fertile & contraception)

Diminished response in non gravid uterine

PGI2 a potent vasodilator and anti-PGF2α

At mid-gestation → PGF2α → tonic contraction

Estrogen stimulate gap junction formation in myometrium

Progesterone inhibit gap junction formation in myometrium

At term → decline in progesterone → gap junction → cyclic

contractions

Estrogen stimulate gap junctions

Progesterone inhibit gap junctions

Gap junction is need for cyclic contraction

Otherwise tonic contraction

Endometrium:

During proliferation: Direct relation between PGE & estradiol

Constriction of spiral arteriols

Suppression of PG synthesis during pregnancy

In pregnancy: less collagen compared with non-pregnant

Decrease in Prog/est ratio ….. More PGE2

Disperse of collagen fibers and replaced with fluid & glycosamin glycan

Make cervix soften

PGE2 dilate cervix at the time of delivery

Inhibits prolactin

Inhibits release of OT

Bind to glucocorticoid receptors on mammary gland

After 34th week…cortisol↑ & CBG↓

As a result ..hCG↓…progesterone↓.►OT↑

Secretion of placental estrogen↑

Sensitivity of uterus to PGF2α↑

Increase pulmonary surfactant

To assist fetus of hypoxia; increase glycogen storage in:

SK.M, heart, liver

PGF2α : control hemorrhage after delivery

In fetus:

Programmed change in HT ››

Increase ACTH ››

Increase cortisol ››

Decrease transcortin ››

Decrease placental progesterone ››

Increase estradiol, OT & PGF2α

PGF2α.... Increase IP3….increase Cain ››

Myometrial contraction

PGE2 . . . . . . Apnea in newborn

PGE2 . . . . . . Lower the resistance of pulmonary vessels

PGE2 . . . . . Stimulate fetal breathing

PGE2 & PGI2 . . . . . Preventing D.A. closure

PGs increase in amniotic fluid during labour

LPA: dilate microvasculature

LPA & LPB: inhibit cytotoxic effects of NK cells

From 5-HPETE

LTD4….. in anaphylaxia

LTB4…… in chemotactic activity

Type Receptor Function

PGI2 IP vasodilation inhibit platelet aggregation bronchodilatation

PGE2

EP1 bronchoconstriction GI tract smooth muscle contraction

EP2 bronchodilatation GI tract smooth muscle relaxation vasodilatation

EP3 ↓ gastric acid secretion ↑ gastric mucus secretion uterus contraction (when pregnant) GI tract smooth muscle contraction lipolysis inhibition ↑ autonomic neurotransmitters ↑ platelet response to their agonists

and ↑ atherothrombosis in vivo

Unspecified hyperalgesia pyrogenic

PGF2α FP uterus contraction bronchoconstriction

Calcium-independent isoform in macrophages

Calcium-dependent isoform in endothelial cells (eNOS)

Neuronal tissues (nNOS) acts as a signal for the development and shaping of

neuronal cells and their activity

control of blood supply to the brain in response to

metabolic demands

Synaptogenesis