HR (Human Reproduction) Lecture Notes: Maternal
Adaptations
Virtually every system changes
Pregnancy is stress test for chronic disease (diabetes, hypertension)
Progesterone receptor expression changes in myometrium for parturition
Principal substrate for feto-placental unit is glucose
Endocrine (see placental hormones in Placentation lecture)
Relaxin (from CL, placenta, decidua)
● Vasodilator
● Softens ligaments, and cervix in late pregnancy
Prolactin (from decidua, maternal pituitary)
● Simulate uterine glands, mammary gland development, nurturing
behaviour
RAAS
CRH (from placenta)
● Suppresses maternal CRH (maternal pituitary is still stimulated by
oestrogen and placental CRH)
● +ve FB (cortisol stimulate CRH production) for more cortisol
production
● More blood glucose since cortisol reduces insulin sensitivity
Cardiovascular
Maternal ABP dips then rises near end
● Initial vasodilation (induces more CO) from relaxin, oestrogen,
progesterone
○ They induce NO and reduce ATII and NA sensitivity
● At the end refractoriness to ATII is lost -> increase in ABP
Increase in CO (greater in twins)
● More SV and HR
○ Eccentric hypertrophy
● Increases early in pregnancy so probably due to vasodilatory CL
hormones not placental
○ Egg donor recipients are at risk then since they don’t have CL
● Distributed to tissues that have increased demand
○ Reproductive tissue, gut (absorption), kidney (excretion), skin
(heat dissipation)
○ Proportion to placenta increases by spiral artery remodelling
● CO changes on position (uterus can compress IVC)
○ Ideal is lying on side, or knee-chest position
Adaptations
Virtually every system changes
Pregnancy is stress test for chronic disease (diabetes, hypertension)
Progesterone receptor expression changes in myometrium for parturition
Principal substrate for feto-placental unit is glucose
Endocrine (see placental hormones in Placentation lecture)
Relaxin (from CL, placenta, decidua)
● Vasodilator
● Softens ligaments, and cervix in late pregnancy
Prolactin (from decidua, maternal pituitary)
● Simulate uterine glands, mammary gland development, nurturing
behaviour
RAAS
CRH (from placenta)
● Suppresses maternal CRH (maternal pituitary is still stimulated by
oestrogen and placental CRH)
● +ve FB (cortisol stimulate CRH production) for more cortisol
production
● More blood glucose since cortisol reduces insulin sensitivity
Cardiovascular
Maternal ABP dips then rises near end
● Initial vasodilation (induces more CO) from relaxin, oestrogen,
progesterone
○ They induce NO and reduce ATII and NA sensitivity
● At the end refractoriness to ATII is lost -> increase in ABP
Increase in CO (greater in twins)
● More SV and HR
○ Eccentric hypertrophy
● Increases early in pregnancy so probably due to vasodilatory CL
hormones not placental
○ Egg donor recipients are at risk then since they don’t have CL
● Distributed to tissues that have increased demand
○ Reproductive tissue, gut (absorption), kidney (excretion), skin
(heat dissipation)
○ Proportion to placenta increases by spiral artery remodelling
● CO changes on position (uterus can compress IVC)
○ Ideal is lying on side, or knee-chest position
