Afroza Khatun

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Parturition

• Presented By
• Afroza Khatun
•          Animal Reproductive Physiology Lab.
•   29 May 2007

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Neuroendocrine Control of Parturition

• Progesterone
• Occurs prior to labor.
• In case of CL dependent-accomplished by uterine
  luteolytic factors (prostaglandin's in some
  species)
• In case of placenta dependent-changes in enzyme
  activities (estrogen , progesterone ,)
• Progesterone is antagonistic to USM, induced
  either by oxytocin or prostaglandin's.
• Lowering of progesterone levels would be the
  stimulus to parturition.

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• Estrogens
• Myometrial excitability ,lowering the membrane
  potential of USM.
• Antagonized activity on myometrium by the action
  of progesterone.
• Uterine estrogen receptors , but progesterone
  levels .
• Enhance uterine excitability by a number of
  mechanisms
• a) endometrial prostaglandin synthetase
  activity.
• b) myometrial and endometrial oxytocin
  receptors
• c) oxytocin production and secretion by the
  neurohypophysis.

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• Prostaglandins
• 1. synthesis and release of prostaglandins
  precede labor.
• 2. Released of progesterone, prostaglandin F2a
  (PGF2a )- corpus luteum.
• 3. Luteal progesterone production is followed by
  uterine contractions and parturition.
• 4. Dependent on stimulation by placental
  estrogens.
• Placental Prolactin
• 1. PRL late gestation, very high in amniotic
  fluid and synthesis by choriondecidual tissue.
• 2. Immunologically similar to pituitary PRL and
  not confused with PL.
• 3. Increased levels of PRL coincide with organ
  of growth fetus and responsible for increased
  growth and function of the fetal adrenal cortex.

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• Autonomic Motor Innervation
• Innervated by adrenergic neurons. (unresolved)
• Both estrogen and progestins -norepinephrine
  content of these nerves as well as as the
  turnover of NE.
• Catacholamine biosynthesis.
• Jap Junction ( nexuses, low-resistance electrical
  pathways)
• are present between the uterine muscles cells.
• Ovarectomy of pregnant animals at midterm causes
  the rapid appearance.
• Is prevented by progesterone administration.
• In preventing electrical communication between
  uterine muscle cells.
• In synchronizing uterine contractility for
  effective expulsion of the fetus.
• Initiated by progesterone withdrawal-
  morphological and functional bases for the
  progesterone block hypothesis formulated much
  earlier by Csapo.

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• Oxytocin
• Neurohypophysial hormone, uterine-contracting
  action.
• Fetal movements monitored and relayed by spinal
  afferents are stimulatory to oxytocin release
  during labor.
• Oxytocin is enhanced by estrogens and depressed
  by progesterone.
• Maternal plasma oxytocin levels increase with
  advancing gestation.
• An initiating factor or only facilitative to
  human labor.
• During gestation plasma estrogen concentrations
  , affinity and number of uterine oxytocin
  receptors.
• Stimulation of endometrial and myometrial
  prostaglandin F2a.
• PGF2astimulate uterine smooth muscle
  cells-contraction of the uterous and expulsion of
  the fetus.

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The Fetal Adrenal Cortex

• Onset of parturition is initiated by the
  activation of the fetal pituitary- adrenal axis.
• Increases in hypertrophy and hyperplasia of
  adrenal cortical cells.
• Premature delivery induced by infusion of ACTH
  or glucocorticoids and prevented by fetal
  adrenalectomy or hypophysectomy.
• Increased fetal glucocorticoid production-stimulat
  e placental production of estrogen from
  progesterone.

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