- Secreted mainly by the anterior pituitary (adenohypophysis).
- Structurally homologous to Growth Hormone (GH).
- Synthesized by lactotroph cells in the anterior pituitary.
Function
| Function | Mechanism / Effect |
|---|---|
| Stimulates milk production | Acts on the mammary glands to promote lactogenesis (milk synthesis) after childbirth. |
| Inhibits ovulation in females | ↓ GnRH → ↓ FSH & LH → anovulation → natural contraception during lactation. |
| Inhibits spermatogenesis in males | ↓ GnRH → ↓ FSH & LH → ↓ testosterone → infertility & low libido. |
Clinical Effects of Excess Prolactin
| In Females | In Males |
|---|---|
| Galactorrhea (milk discharge not related to pregnancy) | Gynecomastia |
| Amenorrhea (absence of menstruation) | Infertility |
| Infertility/anovulation | Decreased libido |
| Osteoporosis (chronic hypogonadism) | Impotence |
Regulation of Prolactin Secretion
| Regulatory Factor | Effect on Prolactin | Mechanism / Clinical Note |
|---|---|---|
| Dopamine (from hypothalamus, tuberoinfundibular pathway) | ↓ Inhibits secretion (tonic inhibition) | Main inhibitory control: Dopamine agonists (e.g., bromocriptine, cabergoline) ↓ , prolactin |
| TRH (Thyrotropin-Releasing Hormone) | ↑ Stimulates secretion | ↑ in primary or secondary hypothyroidism → galactorrhea, amenorrhea |
| Estrogen (OCPs, pregnancy) | ↑ Stimulates secretion | ↑ lactotroph sensitivity and size |
| Dopamine antagonists (antipsychotics, metoclopramide) | ↑ Stimulates secretion | Block D₂ receptors → hyperprolactinemia |
| Prolactin (feedback) | ↓ Inhibits its own secretion | ↑ dopamine synthesis in the hypothalamus |
| Nipple stimulation/infant cry | ↑ Stimulates secretion | Neural input via the spinal cord → hypothalamic inhibition of dopamine |
| Chest wall injury | ↑ Stimulates secretion | Via autonomic reflex → dopamine inhibition |
Feedback Summary Diagram
| Stimulus / Condition | Effect on Prolactin | Mechanism |
|---|---|---|
| Nipple stimulation, suckling | ↑ | ↓ dopamine → ↑ prolactin |
| Hypothyroidism (↑ TRH) | ↑ | TRH stimulates prolactin release |
| Dopamine agonists | ↓ | Stimulate D₂ receptors → inhibit prolactin |
| Dopamine antagonists | ↑ | Block D₂ receptors → increase prolactin |
| Prolactinoma | ↑ | Pituitary adenoma of lactotrophs |
| Pregnancy / Estrogen therapy | ↑ | Estrogen stimulates lactotrophs |
Clinical Correlations
| Condition | Pathophysiology | Key Features | Treatment |
|---|---|---|---|
| Prolactinoma | Pituitary adenoma of lactotrophs | Galactorrhea, amenorrhea, infertility, ↓ libido | Dopamine agonists (bromocriptine, cabergoline) |
| Hypothyroidism | ↑ TRH → ↑ prolactin | Galactorrhea, menstrual irregularity | Treat with levothyroxine |
| Drug-induced hyperprolactinemia | Dopamine antagonists (e.g., antipsychotics) | Galactorrhea, sexual dysfunction | Discontinue/switch drug |
| Renal failure | ↓ prolactin elimination | Hyperprolactinemia symptoms | Manage renal function |
Key Points to Remember
- Dopamine inhibits prolactin (via D₂ receptors).
- TRH and estrogen stimulate prolactin.
- Prolactin inhibits GnRH → infertility and amenorrhea.
- Hyperprolactinemia → galactorrhea and reproductive dysfunction.
- Treatment: Dopamine agonists (bromocriptine, cabergoline).
Learning Objectives
By the end of this topic, you should be able to:
- Describe the source and function of prolactin.
- Explain how dopamine and TRH regulate prolactin secretion.
- Identify clinical features of prolactin excess in males and females.
- Understand the mechanisms and management of hyperprolactinemia.
