Post on 14-Jun-2015
transcript
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