Cortisol secretion pathway

The "cortisol secretion pathway," more accurately known as the hypothalamic-pituitary-adrenal (HPA) axis, describes the neuroendocrine cascade that regulates production and release of cortisol from the adrenal cortex. This begins in response to stress or circadian signals when the hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates CRH receptors on anterior pituitary cells. These cells then secrete adrenocorticotropic hormone (ACTH), which travels through circulation to bind ACTH receptors on adrenal cortical cells—primarily in the zona fasciculata—stimulating enzymatic conversion of cholesterol into cortisol. Cortisol exerts negative feedback at both pituitary and hypothalamic levels by binding intracellular glucocorticoid receptors that regulate gene expression via DNA response elements. This tightly regulated system controls metabolism, immune function, stress adaptation, inflammation suppression, blood pressure maintenance, and more. Dysregulation can result in various diseases including Cushing’s syndrome/disease or Addison’s disease[1][2][3][5][7]. *Note*: For structured databases focused on drug targets or biomolecules rather than pathways/processes, the correct approach would be to list each major protein/receptor/enzyme individually: – Corticotropin-releasing hormone receptor type 1 (CRHR1) – Adrenocorticotropic hormone receptor (MC2R) – Glucocorticoid receptor (NR3C1) If you need information about any specific component within this pathway as a canonical target entry, please specify which one.

Other names

Hypothalamic-pituitary-adrenal axisHPA axisCortisol biosynthesis and release cascade

Mechanisms depend on which component of the pathway is targeted. For example, Glucocorticoids act as agonists at glucocorticoid receptors. Synthesis inhibitors block steroidogenic enzymes in the adrenal cortex. Glucocorticoid receptor antagonists block cortisol binding to glucocorticoid receptors. ACTH analogs or antagonists also affect this system.