What are the hormones produced by the placenta and what are their roles in pregnancy?

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Hormones of the Placenta

The placenta functions as a rich endocrine organ that produces steroids, peptide hormones, growth factors, and cytokines essential for pregnancy maintenance, maternal metabolic adaptation, and fetal development. 1

Major Placental Hormones and Their Functions

Steroid Hormones

Progesterone is synthesized by the placenta and serves multiple critical roles 2:

  • Maintains pregnancy by preventing uterine contractions
  • Mediates vasodilation through reduction in systemic vascular resistance
  • Relaxes gastroesophageal sphincters (increasing aspiration risk in late pregnancy)
  • Increases minute ventilation by 20-40% above baseline by term, producing mild respiratory alkalosis

Estrogens are produced by the fetoplacental unit and contribute to 3:

  • Uterine growth and blood flow expansion
  • Increased COX-2 expression in myometrium (maximal at delivery)
  • Preparation for parturition
  • After delivery, withdrawal of placental estrogens triggers uterine involution

Peptide and Protein Hormones

Human Chorionic Gonadotropin (hCG) 4, 5:

  • Maintains corpus luteum in early pregnancy
  • Supports progesterone production until placenta assumes this role
  • Essential for pregnancy establishment

Human Placental Lactogen (hPL) 6:

  • Increases maternal food intake by inducing central leptin resistance
  • Promotes maternal beta-cell expansion and insulin production
  • Defends against gestational diabetes by supporting insulin secretion
  • Works synergistically with glucose to potentiate metabolic effects

Placental Growth Hormone (GH-V) 1, 6:

  • Replaces pituitary growth hormone during pregnancy
  • Induces maternal insulin resistance (a key driver of pregnancy-induced insulin resistance)
  • Mobilizes maternal nutrients for fetal growth
  • Dysregulation is associated with gestational diabetes mellitus

Vasodilatory Hormones

Relaxin 2:

  • Initially produced by corpus luteum, then by placenta
  • Attenuates pressor response to angiotensin II
  • Contributes to decreased systemic vascular resistance
  • Facilitates development of low-resistance uteroplacental circulation

Brain Natriuretic Peptide (BNP) and NT-proBNP 2:

  • Function as potent vasodilators
  • Found in higher concentrations during first trimester
  • Represent adaptive response to physiologic volume expansion

Angiogenic Factors

Placental Growth Factor (PlGF) 7, 8:

  • Member of vascular endothelial growth factor family
  • Concentrations rise continuously from first trimester until 29-33 weeks, then decline
  • Essential for placental vascular development
  • Low levels associated with placental dysfunction, preeclampsia, and fetal growth restriction

Soluble fms-like tyrosine kinase-1 (sFlt-1) 7, 8:

  • Binds and neutralizes PlGF in circulation
  • Remains stable until 29-33 weeks, then rises steadily until delivery
  • Reflects trophoblast stress
  • Elevated levels precede preeclampsia symptoms by approximately 1 month
  • High sFlt-1/PlGF ratio indicates placental dysfunction

Cytokines and Inflammatory Mediators

TNF-α, Interleukin-6, and Leptin 1:

  • Increased expression in placentas from women with gestational diabetes
  • May contribute to exaggerated insulin resistance in GDM pregnancies
  • Directly affect maternal metabolism and fetal development

Clinical Implications

Metabolic Adaptations

The placental hormones orchestrate profound maternal metabolic changes 6:

  • Placental GH-V and hPL integrate metabolic adaptations with fetal developmental demands
  • These hormones induce physiologic insulin resistance to redirect nutrients to the fetus
  • Dysregulation leads to gestational diabetes when maternal beta-cells cannot compensate

Cardiovascular Changes

Placental hormones drive hemodynamic alterations 2:

  • Blood pressure initially declines due to progesterone and relaxin-mediated vasodilation
  • Systolic and diastolic BP increase by approximately 8 mm Hg by delivery
  • After placental delivery, withdrawal of vasodilatory hormones causes BP to rise, peaking on postpartum days 3-7

Parturition Trigger

Hormonal shifts initiate labor 3:

  • Maximal COX-2 expression stimulates prostaglandin production
  • Estrogen-to-progesterone ratio changes
  • Coordinated withdrawal of pregnancy-maintaining hormones

Common Pitfalls

Avoid assuming all placental hormone production is autonomous - the fetoplacental unit requires precursors from both mother and fetus for steroid synthesis 5, 9

Do not overlook the postpartum period - withdrawal of placental hormones after delivery causes rapid physiologic changes, including BP elevation and metabolic shifts that require monitoring 2

Recognize that placental hormone dysregulation has long-term consequences - abnormal levels during pregnancy are associated with future cardiovascular disease risk and metabolic dysfunction in the mother 2

References

5
Research

The endocrine function of human placenta: an overview.

Reproductive biomedicine online, 2016

6
Research

Placental hormones and the control of maternal metabolism and fetal growth.

Current opinion in endocrinology, diabetes, and obesity, 2011

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