Endocrine

Lipophilic hormones — steroid hormones (cortisol, aldosterone, sex steroids), thyroid hormone, and vitamin D. They diffuse across the membrane and bind intracellular receptors that act as transcription factors, giving a slow, sustained genomic response.

cAMP. Gs activates adenylyl cyclase (raising cAMP → activates protein kinase A); Gi inhibits adenylyl cyclase (lowering cAMP). Examples of Gs: glucagon, ACTH, FSH, LH, TSH, PTH, calcitonin, GHRH, ADH (V2).

Gq activates phospholipase C → cleaves PIP2 into IP3 and DAG. IP3 raises intracellular Ca2+; DAG activates protein kinase C. Examples: GnRH, TRH, histamine (H1), angiotensin II, ADH (V1), oxytocin, α1-adrenergic, M1/M3. (GHRH is Gs-coupled, not Gq.)

Insulin, IGF-1, and most growth factors use intrinsic receptor tyrosine kinases (MAP kinase / PI3K pathways). Prolactin, GH, leptin, erythropoietin, and most cytokines use JAK/STAT (non-receptor tyrosine kinase) pathways. Atrial natriuretic peptide uses guanylyl cyclase (cGMP).

The peripheral hormone (e.g., cortisol, thyroid hormone) inhibits both the hypothalamic releasing hormone and the anterior pituitary trophic hormone, reducing further stimulation. This keeps hormone levels within a set range and underlies the use of paired hormone levels to localize disease.

ADH (vasopressin) and oxytocin. Both are synthesized in hypothalamic neurons (supraoptic and paraventricular nuclei) and transported down axons for storage/release in the posterior pituitary (neurohypophysis). The posterior pituitary makes no hormones itself.