Hormones Secreted by the Pituitary Gland

Why This Matters

The pituitary gland earns its nickname as the "master gland" because it orchestrates hormone release throughout your entire body. What you're really being tested on, though, are the feedback loops and target organ relationships that keep these systems in balance. Understanding pituitary hormones means understanding how the hypothalamus communicates with peripheral glands, how negative feedback maintains homeostasis, and what happens when these systems fail. These concepts show up in questions about endocrine pathology, reproductive physiology, fluid balance, and stress responses.

Don't just memorize which hormone does what. Know which lobe secretes it, what releases or inhibits it, and what target tissue responds. The pituitary is divided into the anterior lobe (adenohypophysis) and posterior lobe (neurohypophysis), and this distinction matters for understanding both hormone synthesis and clinical disorders.

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Anterior Pituitary: Tropic Hormones

Tropic hormones act on other endocrine glands to stimulate hormone release. Think of them as relay signals: the hypothalamus sends a releasing hormone to the anterior pituitary, which then sends a tropic hormone to a peripheral gland.

Adrenocorticotropic Hormone (ACTH)

• Stimulates the adrenal cortex to release cortisol, the body's primary glucocorticoid for the stress response
• Regulated by CRH (corticotropin-releasing hormone) from the hypothalamus and inhibited by cortisol via negative feedback
• Clinical relevance: Excess ACTH from a pituitary adenoma causes Cushing's disease; deficiency leads to secondary adrenal insufficiency (distinguished from primary because the problem is upstream of the adrenal gland itself)

Thyroid-Stimulating Hormone (TSH)

• Targets thyroid follicular cells to promote synthesis and release of $T_3$ and $T_4$
• Controlled by TRH (thyrotropin-releasing hormone) and inhibited by circulating thyroid hormones
• Diagnostic marker: Elevated TSH with low $T_3$/$T_4$ indicates primary hypothyroidism (the thyroid itself is failing, so the pituitary ramps up TSH). Suppressed TSH with high $T_3$/$T_4$ suggests hyperthyroidism (excess thyroid hormone shuts down TSH via negative feedback).

Follicle-Stimulating Hormone (FSH)

• Promotes follicle development in ovaries and supports spermatogenesis in the seminiferous tubules of the testes
• Works synergistically with LH. Both are gonadotropins released in response to pulsatile GnRH (gonadotropin-releasing hormone) from the hypothalamus.
• Inhibited by inhibin from the gonads, providing sex-specific negative feedback

Luteinizing Hormone (LH)

• Triggers ovulation and stimulates corpus luteum formation in females; drives testosterone production by Leydig cells in males
• The mid-cycle LH surge is essential for ovulation. This is a classic exam topic in reproductive physiology and a notable example of positive feedback: rising estrogen from the maturing follicle eventually stimulates (rather than inhibits) LH release once it crosses a threshold.
• Pulsatile secretion pattern is critical. Continuous GnRH actually suppresses LH release by downregulating GnRH receptors on the anterior pituitary. This principle is used clinically with GnRH agonists (like leuprolide) to treat conditions like endometriosis and prostate cancer.

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Anterior Pituitary: Direct-Acting Hormones

These hormones act directly on non-endocrine target tissues rather than stimulating other glands.

Growth Hormone (GH)

• Stimulates linear growth by promoting IGF-1 (insulin-like growth factor 1) release from the liver. IGF-1 then acts on bone epiphyseal plates to drive lengthening.
• Metabolic effects include increased protein synthesis, lipolysis (fat breakdown), and insulin resistance. This insulin-opposing action is called the diabetogenic effect.
• Secretion peaks during deep sleep and is stimulated by GHRH (growth hormone-releasing hormone). It's inhibited by somatostatin (also called GHIH) from the hypothalamus.
• Clinical relevance: Excess GH before epiphyseal plate closure causes gigantism; excess after closure causes acromegaly. Deficiency in children results in pituitary dwarfism.

Prolactin (PRL)

• Stimulates mammary gland development and milk synthesis during lactation
• Uniquely inhibited at baseline. Dopamine from the hypothalamus tonically suppresses prolactin release. This means that severing the connection between the hypothalamus and pituitary (e.g., from a stalk lesion) increases prolactin, unlike every other anterior pituitary hormone, which would decrease.
• Hyperprolactinemia causes galactorrhea (inappropriate milk production) and amenorrhea; it often results from pituitary adenomas or dopamine-blocking drugs (like certain antipsychotics)

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Anterior Pituitary: Melanocyte Regulation

Melanocyte-Stimulating Hormone (MSH)

• Stimulates melanocytes to produce and disperse melanin, increasing skin pigmentation
• Derived from POMC (proopiomelanocortin), the same precursor molecule that produces ACTH

The shared POMC origin has an important clinical connection: in primary adrenal insufficiency (Addison's disease), low cortisol removes negative feedback, so the anterior pituitary produces large amounts of POMC. This increases both ACTH and MSH, which is why patients with Addison's disease develop characteristic hyperpigmentation, especially in skin creases, gums, and scars.

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Posterior Pituitary: Neurohypophyseal Hormones

The posterior pituitary doesn't synthesize hormones. Instead, it stores and releases hormones made by neurons in the hypothalamus. These are true neurohormones, synthesized in hypothalamic cell bodies and transported down axons to the posterior lobe for release into the blood.

Antidiuretic Hormone (ADH) / Vasopressin

• Increases water reabsorption by inserting aquaporin-2 channels into the apical membrane of collecting duct principal cells in the kidneys
• Released in response to increased plasma osmolarity (detected by hypothalamic osmoreceptors) or decreased blood volume/pressure (detected by baroreceptors)
• Clinical disorders: Diabetes insipidus (ADH deficiency or receptor insensitivity) causes large volumes of dilute urine and excessive thirst. SIADH (excess ADH secretion) causes water retention and dilutional hyponatremia.
• At higher concentrations, ADH also acts as a vasoconstrictor (hence the name vasopressin), which helps raise blood pressure

Oxytocin

• Triggers uterine smooth muscle contraction during labor and myoepithelial cell contraction for milk ejection (letdown reflex)
• Operates via positive feedback during labor: uterine contractions push the fetus against the cervix, stimulating more oxytocin release, which causes stronger contractions. This cycle continues until delivery.
• Synthesized in the paraventricular and supraoptic nuclei of the hypothalamus, then transported to the posterior pituitary for storage and release

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Quick Reference Table

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Self-Check Questions

1. Which two anterior pituitary hormones share a common precursor molecule, and how does this explain hyperpigmentation in Addison's disease?

2. Compare and contrast FSH and LH: What target cells does each act on in males, and how do their functions differ?

3. A patient presents with dilute urine and excessive thirst despite adequate fluid intake. Which pituitary hormone is likely deficient, and what receptor mechanism is impaired?

4. Why does continuous GnRH administration suppress gonadotropin release, even though pulsatile GnRH stimulates it? How is this principle used clinically?

5. A prolactin-secreting pituitary tumor causes both galactorrhea and infertility. What two mechanisms explain these symptoms? (Hint: think about what high prolactin does to GnRH.)