Pharmacology of Hypothalamic and Pituitary Hormones

Introduction/Overview

The hypothalamic-pituitary axis represents the principal regulatory interface between the neural and endocrine systems, orchestrating a wide array of physiological processes including growth, metabolism, reproduction, stress response, and fluid balance. The pharmacology of hormones derived from or targeting this axis constitutes a cornerstone of endocrinology and therapeutics. This chapter examines the pharmacological principles governing natural hormones, their synthetic analogs, and antagonists used in clinical medicine. A thorough understanding of these agents is essential for managing endocrine disorders, certain cancers, and reproductive health conditions.

The clinical relevance of these pharmacological agents is profound. They are employed not only for hormone replacement in deficiency states but also for diagnostic purposes, suppression of pathological hormone secretion, and treatment of hormone-sensitive malignancies. The development of recombinant DNA technology has revolutionized this field, enabling the production of pure, non-antigenic hormones that are structurally identical to their human counterparts, thereby expanding therapeutic possibilities and improving safety profiles.

Learning Objectives

• Classify the major pharmacological agents derived from or acting on the hypothalamic-pituitary axis based on their origin, structure, and primary therapeutic action.
• Explain the molecular mechanisms of action for hypothalamic releasing hormones, anterior and posterior pituitary hormones, and their respective antagonists.
• Analyze the pharmacokinetic properties of these hormones, including routes of administration, distribution, metabolism, and elimination, and relate these to their clinical dosing regimens.
• Evaluate the approved therapeutic applications, major adverse effects, and significant drug interactions associated with these pharmacological agents.
• Apply knowledge of special considerations, including use in pregnancy, pediatrics, geriatrics, and organ impairment, to optimize therapeutic decision-making.

Classification

Pharmacological agents related to the hypothalamic-pituitary axis can be systematically classified based on their site of origin, chemical nature, and primary pharmacological action. This classification provides a framework for understanding their therapeutic roles and mechanisms.

Hypothalamic Releasing and Inhibiting Hormones

These are peptides synthesized in hypothalamic neurons and secreted into the hypophyseal portal system to regulate anterior pituitary function. Their synthetic analogs and antagonists are used clinically.

• Gonadotropin-Releasing Hormone (GnRH) Agonists: Leuprolide, goserelin, histrelin, nafarelin.
• GnRH Antagonists: Ganirelix, cetrorelix, degarelix.
• Growth Hormone-Releasing Hormone (GHRH) Analog: Tesamorelin.
• Somatostatin Analogs: Octreotide, lanreotide, pasireotide.
• Dopamine Agonists (acting on pituitary lactotrophs): Bromocriptine, cabergoline.

Anterior Pituitary Hormones and Analogs

These hormones are secreted by the adenohypophysis in response to hypothalamic signals. Recombinant forms are used for replacement therapy.

• Growth Hormone (GH) / Somatotropin: Somatropin (recombinant human GH).
• Gonadotropins:
  • Follicle-Stimulating Hormone (FSH): Follitropin alfa, follitropin beta.
  • Luteinizing Hormone (LH): Lutropin alfa.
  • Human Chorionic Gonadotropin (hCG, LH-like activity): Chorionic gonadotropin (recombinant or urinary).
  • Menotropins (urinary-derived FSH and LH).
• Thyroid-Stimulating Hormone (TSH) / Thyrotropin: Recombinant human TSH (thyrotropin alfa).
• Adrenocorticotropic Hormone (ACTH) / Corticotropin: Cosyntropin (synthetic ACTH analog for diagnosis).
• Prolactin: Rarely used therapeutically; pharmacological focus is on suppression via dopamine agonists.

Posterior Pituitary Hormones and Analogs

These nonapeptides are synthesized in the hypothalamus and stored/released from the neurohypophysis.

• Antidiuretic Hormone (ADH, Vasopressin) Analogs:
  • Agonists: Vasopressin, desmopressin, terlipressin.
  • Antagonists (Vaptans): Conivaptan, tolvaptan.
• Oxytocin and Analogs: Oxytocin, carbetocin.

Mechanism of Action

The pharmacodynamic actions of hypothalamic and pituitary hormones are mediated through specific, high-affinity interactions with cell surface receptors, predominantly G protein-coupled receptors (GPCRs). The subsequent intracellular signaling cascades dictate the physiological and therapeutic effects.

Hypothalamic Hormone Pharmacology

GnRH Agonists and Antagonists: Endogenous GnRH binds to the GnRH receptor, a GPCR on anterior pituitary gonadotrophs, activating the G_q pathway. This leads to phospholipase C activation, inositol trisphosphate (IP₃) production, and calcium mobilization, ultimately stimulating the synthesis and pulsatile release of LH and FSH. Continuous administration of GnRH agonists (e.g., leuprolide) causes profound downregulation and desensitization of the GnRH receptor, leading to suppression of gonadotropin secretion and a hypogonadal state. In contrast, GnRH antagonists (e.g., ganirelix) competitively block the receptor without initial stimulation, providing immediate suppression.

Somatostatin Analogs: Somatostatin exerts inhibitory effects on multiple endocrine cells by activating a family of GPCRs (SSTR_1-5). Octreotide and lanreotide have high affinity for SSTR₂ and SSTR₅. Receptor activation leads to inhibition of adenylate cyclase (via G_i), reduction in intracellular cAMP, and modulation of calcium and potassium channels. This results in suppressed secretion of GH, TSH, glucagon, insulin, and various gastrointestinal hormones.

Dopamine Agonists: Bromocriptine and cabergoline are ergot-derived agonists at dopamine D₂ receptors. On pituitary lactotrophs, D₂ receptor activation inhibits adenylate cyclase and calcium influx, leading to decreased synthesis and secretion of prolactin.

Anterior Pituitary Hormone Pharmacology

Growth Hormone (Somatropin): GH acts by binding to the transmembrane GH receptor, a member of the cytokine receptor superfamily. Receptor dimerization activates the intracellular JAK2 (Janus kinase 2) pathway, leading to phosphorylation of STAT (Signal Transducer and Activator of Transcription) proteins. This regulates gene transcription for insulin-like growth factor-1 (IGF-1) production, primarily in the liver. The anabolic, growth-promoting effects of GH are largely mediated through systemic and local IGF-1.

Gonadotropins (FSH, LH, hCG): These hormones act via GPCRs. The FSH receptor and LH/hCG receptor are coupled primarily to G_s proteins, stimulating adenylate cyclase and increasing intracellular cAMP. In the ovary, FSH promotes follicular development and estrogen synthesis, while LH triggers ovulation and supports the corpus luteum. In the testes, FSH supports spermatogenesis via Sertoli cells, and LH stimulates testosterone production from Leydig cells.

Thyrotropin (TSH): TSH binds to the TSH receptor on thyroid follicular cells, a GPCR coupled to both G_s and G_q proteins. Activation stimulates cAMP production (via G_s) and the phosphoinositide pathway (via G_q), leading to increased thyroid hormone synthesis, secretion, and thyroid gland growth.

Posterior Pituitary Hormone Pharmacology

Vasopressin Analogs: Vasopressin acts on three GPCR subtypes: V_1a (vascular smooth muscle, causing vasoconstriction), V_1b (pituitary, modulating ACTH release), and V₂ (renal collecting duct). The V₂ receptor is coupled to G_s protein. Activation stimulates adenylate cyclase, increasing cAMP, which leads to the insertion of aquaporin-2 water channels into the luminal membrane, promoting water reabsorption. Desmopressin is a selective V₂ receptor agonist. Vaptans (e.g., tolvaptan) are selective V₂ receptor antagonists that promote aquaresis.

Oxytocin: Oxytocin acts on the oxytocin receptor, a GPCR coupled to G_q. Activation stimulates phospholipase C, generating IP₃ and diacylglycerol (DAG), leading to increased intracellular calcium. In uterine myometrium, this causes contraction. In mammary myoepithelial cells, it causes milk ejection.

Pharmacokinetics

The pharmacokinetic profiles of peptide and protein hormones are characterized by poor oral bioavailability due to extensive proteolytic degradation in the gastrointestinal tract. Consequently, most are administered via parenteral or specialized non-oral routes.

Absorption

Parenteral Administration: Subcutaneous (SC) and intramuscular (IM) injections are the most common routes for hormones like somatropin, gonadotropins, and somatostatin analogs. Absorption from these sites is generally slow and variable, influenced by factors such as injection depth, site vascularity, and molecular size. For example, the bioavailability of SC somatropin is approximately 70-90%.

Specialized Delivery Systems: Several agents utilize advanced delivery to improve compliance or pharmacokinetics. Long-acting depot formulations (e.g., leuprolide acetate depot, lanreotide Autogel®) provide sustained release over weeks or months. Intranasal administration is effective for small peptides like desmopressin (nasal spray) and nafarelin, though bioavailability is low (≈3-5%) and variable. Oral formulations exist for non-peptide agents like dopamine agonists (bromocriptine, cabergoline), which are well-absorbed.

Distribution

Distribution volumes for these hormones typically approximate the extracellular fluid volume or plasma volume due to their large molecular size and hydrophilic nature. For instance, the volume of distribution of somatropin is about 0.1 L/kg. They generally do not cross the blood-brain barrier readily. Binding to plasma proteins is variable; growth hormone-binding protein (GHBP) binds a portion of circulating GH, while other hormones like vasopressin have minimal protein binding.

Metabolism and Elimination

Peptide hormones are primarily metabolized by proteolytic cleavage in the liver, kidneys, and at the site of administration. Renal and hepatic clearance are significant pathways. For example, vasopressin and oxytocin are rapidly inactivated by peptidases in the liver and kidney, resulting in very short plasma half-lives (5-20 minutes). Modifications to the natural peptide structure, such as in desmopressin (deamination and D-arginine substitution), confer resistance to enzymatic degradation, prolonging the half-life to 2-4 hours. Recombinant hormones like somatropin are cleared via receptor-mediated endocytosis and subsequent lysosomal degradation, with significant renal filtration of smaller fragments.

Half-life and Dosing Considerations

The elimination half-life (t_1/2) is a critical determinant of dosing frequency.

• Short t_1/2 (minutes): Native vasopressin, oxytocin, cosyntropin. Require continuous IV infusion or frequent dosing for sustained effect.
• Intermediate t_1/2 (hours): Subcutaneous somatropin (t_1/2 ≈ 3-5 hours), SC octreotide (t_1/2 ≈ 1.5-2 hours), leading to daily or multiple-daily dosing.
• Long t_1/2 (days to weeks): Long-acting formulations are designed for less frequent administration. Cabergoline (oral) has a terminal t_1/2 of ≈65 hours, allowing twice-weekly dosing. Depot leuprolide (1-6 month formulations) and lanreotide Autogel® (4-week formulation) provide sustained release from a biodegradable matrix.

Dosing is often individualized based on clinical response, serum hormone levels (e.g., IGF-1 for GH therapy), or weight/body surface area, particularly in pediatric populations.

Therapeutic Uses/Clinical Applications

The clinical applications of these agents span diagnostic testing, hormone replacement, suppression of pathological secretion, and treatment of non-endocrine conditions.

Diagnostic Applications

• Cosyntropin Stimulation Test: The standard test for assessing adrenal insufficiency. Cosyntropin (synthetic ACTH_1-24) is administered, and cortisol response is measured.
• Recombinant Human TSH (Thyrotropin Alfa): Used to stimulate radioactive iodine uptake and thyroglobulin production in the follow-up of differentiated thyroid cancer, avoiding the need for thyroid hormone withdrawal and resultant hypothyroidism.
• GnRH Stimulation Test: Administration of native GnRH (gonadorelin) can help differentiate hypothalamic from pituitary causes of hypogonadism by assessing LH and FSH response.

Hormone Replacement Therapy

• Growth Hormone Deficiency: Somatropin is indicated in children for growth failure due to GH deficiency, Turner syndrome, chronic renal insufficiency, and Prader-Willi syndrome. In adults with severe GH deficiency, it improves body composition, lipid profile, and quality of life.
• Diabetes Insipidus: Desmopressin, a selective V₂ agonist, is the mainstay for central diabetes insipidus, administered intranasally, orally, or subcutaneously.
• Hypogonadotropic Hypogonadism: Gonadotropins (hCG ± FSH) or pulsatile GnRH are used to induce spermatogenesis and testosterone production in men, and ovulation in women.

Suppression of Hormone Secretion or Action

• Central Precocious Puberty: GnRH agonists (e.g., leuprolide) suppress the pituitary-gonadal axis, halting premature sexual development.
• Hormone-Sensitive Cancers: GnRH agonists and antagonists are used for androgen deprivation in prostate cancer and for creating a hypoestrogenic state in premenopausal hormone receptor-positive breast cancer.
• Acromegaly: Somatostatin analogs (octreotide, lanreotide) are first-line medical therapy to reduce GH and IGF-1 levels. Pegvisomant, a GH receptor antagonist, is used in cases resistant to somatostatin analogs.
• Hyperprolactinemia: Dopamine agonists (cabergoline, bromocriptine) are first-line therapy for prolactinomas and idiopathic hyperprolactinemia, effectively normalizing prolactin levels and reducing tumor size.
• Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): Vaptans (tolvaptan, conivaptan) are used to promote aquaresis and correct hyponatremia.

Reproductive Medicine

• Ovulation Induction: Gonadotropins (FSH, LH, hCG) are central to assisted reproductive technologies (ART) for controlled ovarian stimulation.
• In Vitro Fertilization (IVF) Cycle Management: GnRH agonists are used for pituitary down-regulation prior to stimulation, while GnRH antagonists are used to prevent a premature LH surge during stimulation.
• Labor Induction and Postpartum Hemorrhage: Oxytocin is administered intravenously to induce or augment labor and to promote uterine contraction after delivery to control bleeding.

Adverse Effects

Adverse effects range from predictable extensions of pharmacological action to immunogenic reactions and formulation-specific issues.

Common Side Effects

• GnRH Agonists/Antagonists: Symptoms of hypoestrogenism or hypoandrogenism: hot flashes, night sweats, decreased libido, vaginal dryness, mood swings, bone mineral density loss with long-term use. Initial flare reaction (worsening of symptoms) can occur with agonists due to transient gonadotropin surge.
• Growth Hormone: Fluid retention (edema, arthralgia, carpal tunnel syndrome), insulin resistance, hyperglycemia, myalgia, headache. In children, slipped capital femoral epiphysis and progression of scoliosis are potential concerns.
• Gonadotropins: Ovarian hyperstimulation syndrome (OHSS), a potentially serious complication characterized by ovarian enlargement, ascites, and hemodynamic instability. Multiple pregnancies, injection site reactions, and breast tenderness are also common.
• Somatostatin Analogs: Gastrointestinal effects (nausea, abdominal pain, diarrhea, steatorrhea), gallstone formation due to inhibition of gallbladder contraction, glucose intolerance (inhibition of insulin secretion), and injection site pain.
• Dopamine Agonists: Nausea, vomiting, orthostatic hypotension, headache, nasal congestion. Less commonly, impulse control disorders (pathological gambling, hypersexuality) and, with ergot derivatives, pleural and retroperitoneal fibrosis.
• Vasopressin Analogs: Desmopressin can cause hyponatremia and water intoxication if fluid intake is not restricted. Headache and facial flushing are common. Terlipressin and vasopressin can cause systemic vasoconstriction, leading to hypertension, peripheral ischemia, and abdominal cramping.
• Oxytocin: Uterine hyperstimulation (tachysystole), which can compromise fetal oxygenation. Water intoxication with prolonged high-dose IV infusion due to its mild antidiuretic effect, hypotension with rapid IV bolus.

Serious/Rare Adverse Reactions and Black Box Warnings

• Increased Mortality in Critical Illness: Somatropin carries a black box warning against use in patients with acute critical illness due to complications following open heart or abdominal surgery, multiple accidental trauma, or acute respiratory failure, as studies showed increased mortality.
• Intracranial Hypertension (Pseudotumor Cerebri): Associated with growth hormone therapy, particularly in children. Symptoms include papilledema, headache, visual changes.
• Neoplasm Risk: There is an ongoing concern and monitoring for second neoplasms in children treated with GH, particularly those with prior risk factors. A black box warning exists regarding the increased risk of malignancy in patients treated with recombinant human TSH (thyrotropin alfa) in the setting of metastatic thyroid cancer.
• Severe Liver Injury: Tolvaptan carries a black box warning for the risk of serious and potentially fatal liver injury when used for autosomal dominant polycystic kidney disease (ADPKD), requiring monitoring.
• Anaphylaxis: Although rare with recombinant products, anaphylactic reactions have been reported with gonadotropins and other protein hormones.

Drug Interactions

Interactions can occur through pharmacokinetic or pharmacodynamic mechanisms, often related to additive hormonal effects or alterations in metabolic clearance.

Major Pharmacodynamic Interactions

• Glucocorticoids: Can antagonize the growth-promoting effects of somatropin and may exacerbate the glucose intolerance caused by both GH and somatostatin analogs.
• Insulin and Oral Hypoglycemics: Somatropin can induce insulin resistance, potentially increasing insulin requirements. Somatostatin analogs can alter glycemic control by suppressing insulin and glucagon secretion, necessitating careful monitoring.
• Other Vasoactive Agents: Vasopressin or terlipressin may have additive pressor effects with other vasoconstrictors, increasing the risk of severe hypertension or ischemia. Conversely, their effects may be antagonized by vasodilators.
• Drugs Affecting Prolactin Secretion: Dopamine antagonists (typical antipsychotics, metoclopramide) can counteract the therapeutic effect of bromocriptine or cabergoline in hyperprolactinemia.
• Cyclosporine: Octreotide may reduce cyclosporine levels, potentially compromising transplant immunosuppression.

Major Pharmacokinetic Interactions

• Enzyme Inducers/Inhibitors: Cabergoline and bromocriptine are metabolized by hepatic CYP3A4. Strong CYP3A4 inhibitors (e.g., ketoconazole, protease inhibitors) can increase their plasma concentrations and toxicity (hypotension, nausea). Inducers (e.g., rifampin) may reduce efficacy.
• Drugs Causing SIADH: Concurrent use of desmopressin with drugs that stimulate vasopressin release or potentiate its effect (e.g., tricyclic antidepressants, SSRIs, carbamazepine, oxcarbazepine, NSAIDs) significantly increases the risk of severe hyponatremia.

Contraindications

• Absolute Contraindications:
  • Active malignancy for growth hormone therapy (exceptions for approved indications like GH deficiency after cancer treatment).
  • Hypersensitivity to the drug or its components.
  • Closed epiphyses (for growth promotion with somatropin).
  • Diabetic retinopathy for GH therapy (risk of progression).
  • Obstructive uropathy or severe renal impairment for desmopressin (risk of fluid overload).
  • Uncontrolled hypertension or coronary artery disease for vasopressin/terlipressin.
  • Hypersensitivity to natural rubber latex (for some multidose vial diaphragms).
• Relative Contraindications: Pregnancy (for many agents, see Special Considerations), severe obesity or history of upper airway obstruction/sleep apnea for GH therapy (risk of worsening), history of psychosis for dopamine agonists.

Special Considerations

Use in Pregnancy and Lactation

Most hypothalamic and pituitary hormones are classified as FDA Pregnancy Category B or C, indicating inadequate human studies or evidence of risk in animal studies. Their use is generally avoided unless the potential benefit justifies the potential risk to the fetus.

• GnRH Agonists/Antagonists: Contraindicated in pregnancy (Category X for some, like leuprolide). They induce a hypogonadal state incompatible with maintaining a pregnancy.
• Oxytocin: Widely used for labor induction/augmentation and postpartum hemorrhage. It crosses the placenta but is considered safe when used as indicated. It is compatible with breastfeeding.
• Desmopressin: Category B. Considered relatively safe for use in pregnancy for treatment of central diabetes insipidus. Minimal transfer into breast milk.
• Dopamine Agonists (Bromocriptine): Category B. Bromocriptine has been used to treat prolactinomas during pregnancy, though typically discontinued once pregnancy is confirmed. Cabergoline data are more limited. They suppress lactation.
• Somatostatin Analogs, Growth Hormone, Gonadotropins: Generally discontinued during pregnancy due to limited safety data.

Pediatric Considerations

Dosing is frequently weight-based or body surface area-based. Monitoring for growth velocity, bone age advancement (with GH or sex steroids), and pubertal development is critical.

• Growth Hormone: Treatment for pediatric GH deficiency requires careful monitoring of growth velocity, IGF-1 levels, and for adverse effects like slipped capital femoral epiphysis or scoliosis progression. Dosing is weight-based (mg/kg/day).
• GnRH Agonists for Precocious Puberty: Treatment aims to halt pubertal progression and delay bone age advancement. Monitoring includes pubertal staging, growth velocity, and periodic bone age X-rays.
• Desmopressin for Nocturnal Enuresis: Used at lower doses than for diabetes insipidus. Fluid intake must be strictly restricted in the evening to prevent hyponatremia.

Geriatric Considerations

Age-related declines in renal and hepatic function can alter the pharmacokinetics of these agents, necessitating dose adjustments.

• Increased Sensitivity: Older adults may be more sensitive to the effects of vasopressin analogs (hyponatremia, fluid overload) and dopamine agonists (orthostatic hypotension, confusion).
• Bone Health: Long-term use of GnRH agonists in elderly men for prostate cancer significantly accelerates bone loss, increasing fracture risk. Concomitant use of bone-protective agents (bisphosphonates, denosumab) is often recommended.
• Dosing: For drugs cleared renally (e.g., desmopressin), doses may need reduction in the setting of age-related reduced creatinine clearance, even with normal serum creatinine.

Renal and Hepatic Impairment

Renal Impairment: Peptide hormones cleared renally (e.g., somatropin, desmopressin) may have reduced clearance, potentially leading to accumulation and increased effects or toxicity. For desmopressin, the risk of water intoxication and severe hyponatremia is markedly increased in patients with chronic kidney disease or those on dialysis. Dose reduction and strict fluid monitoring are essential. Vaptans are contraindicated in anuric patients.

Hepatic Impairment: The liver is a major site of peptide metabolism. Impairment may prolong the half-life of hormones like vasopressin, somatostatin analogs, and metabolized dopamine agonists. For octreotide and lanreotide, dosage adjustment is not typically required, but caution is advised. In cirrhosis with ascites, the use of V₂ antagonists (tolvaptan) requires extreme caution due to the risk of overly rapid correction of hyponatremia and its complications (osmotic demyelination).

Summary/Key Points

• The hypothalamic-pituitary hormones and their pharmacological analogs act primarily through specific G protein-coupled receptors or cytokine receptors, initiating intracellular signaling cascades that regulate growth, metabolism, reproduction, and fluid balance.
• Due to their peptide nature, most agents have poor oral bioavailability and are administered via subcutaneous, intramuscular, or specialized routes (intranasal, depot formulations). Pharmacokinetics are characterized by proteolytic metabolism and renal/hepatic clearance.
• Major therapeutic classes include: hormone replacement agents (somatropin, desmopressin, gonadotropins), secretion suppressors (somatostatin analogs, dopamine agonists), axis modulators (GnRH agonists/antagonists for cancer or puberty), and posterior pituitary agents (oxytocin, vaptans).
• Adverse effects are often extensions of pharmacological action: fluid retention with GH, hypoestrogenism with GnRH agonists, ovarian hyperstimulation with gonadotropins, hyponatremia with desmopressin, and GI upset with somatostatin analogs. Serious risks include increased mortality in critical illness (GH) and liver injury (tolvaptan).
• Significant drug interactions occur via pharmacodynamic additivity (e.g., vasoconstrictors with vasopressin) or pharmacokinetic modulation of CYP3A4-metabolized agents (dopamine agonists).
• Special populations require tailored approaches: cautious use in pregnancy/lactation, weight-based dosing in pediatrics with growth monitoring, attention to bone health and fall risk in geriatrics, and dose adjustment in renal/hepatic impairment to prevent toxicity.

Clinical Pearls

• The “flare phenomenon” seen with initial GnRH agonist therapy can be clinically managed in prostate cancer with concurrent antiandrogen administration for the first few weeks.
• When monitoring GH therapy, serum IGF-1 levels are a more stable indicator of biological activity than pulsatile GH levels and should be maintained in the age-adjusted normal range.
• For patients on desmopressin, a crucial component of counseling is strict fluid intake restriction to prevent iatrogenic hyponatremia, which can be life-threatening.
• In acromegaly, first-generation somatostatin analogs (octreotide, lanreotide) are most effective against tumors expressing SSTR₂, while pasireotide has broader receptor affinity and may be considered in selected cases.
• The choice between a GnRH agonist and antagonist in assisted reproduction involves balancing the need for precise cycle control (antagonists allow a shorter protocol) with potential differences in endometrial receptivity and cost.

References

1. Whalen K, Finkel R, Panavelil TA. Lippincott Illustrated Reviews: Pharmacology. 7th ed. Philadelphia: Wolters Kluwer; 2019.
2. Rang HP, Ritter JM, Flower RJ, Henderson G. Rang & Dale's Pharmacology. 9th ed. Edinburgh: Elsevier; 2020.
3. Trevor AJ, Katzung BG, Kruidering-Hall M. Katzung & Trevor's Pharmacology: Examination & Board Review. 13th ed. New York: McGraw-Hill Education; 2022.
4. Brunton LL, Hilal-Dandan R, Knollmann BC. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 14th ed. New York: McGraw-Hill Education; 2023.
5. Katzung BG, Vanderah TW. Basic & Clinical Pharmacology. 15th ed. New York: McGraw-Hill Education; 2021.
6. Golan DE, Armstrong EJ, Armstrong AW. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 4th ed. Philadelphia: Wolters Kluwer; 2017.
7. Whalen K, Finkel R, Panavelil TA. Lippincott Illustrated Reviews: Pharmacology. 7th ed. Philadelphia: Wolters Kluwer; 2019.
8. Rang HP, Ritter JM, Flower RJ, Henderson G. Rang & Dale's Pharmacology. 9th ed. Edinburgh: Elsevier; 2020.

⚠️ Medical Disclaimer

This article is intended for educational and informational purposes only. It is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this article.

The information provided here is based on current scientific literature and established pharmacological principles. However, medical knowledge evolves continuously, and individual patient responses to medications may vary. Healthcare professionals should always use their clinical judgment when applying this information to patient care.

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Mentor, Pharmacology. Pharmacology of Hypothalamic and Pituitary Hormones. Pharmacology Mentor. Available from: https://pharmacologymentor.com/pharmacology-of-hypothalamic-and-pituitary-hormones/. Accessed on February 8, 2026 at 08:46.
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