Adrenal Gland Function: Study Notes (ACBS 400A/500A)
Structure of Adrenal Gland
- Two bean-shaped endocrine organs that secrete various hormones
- Located near the cranial pole of the kidneys; Right gland is positioned slightly more cranial than the left
- Surrounded by a thick capsule
Cortex vs Medulla
- Adrenal gland has two main compartments:
- Cortex (outer layer)
- Medulla (inner core)
Cortex: Zona Glomerulosa
- Outermost layer of the cortex
- Produces mineralocorticoid aldosterone
- Aldosterone helps regulate electrolyte balance
- Histology: tight trabecular clusters of polygonal cells with moderate eosinophilic, slightly vacuolated cytoplasm and round nuclei
- Minimal response to ACTH
Cortex: Zona Fasciculata
- Central layer; thickest of the three cortical layers
- Produces glucocorticoids: cortisol and corticosterone
- Cortisol (in most species) with corticosterone in some species
- Roles in glucose metabolism and stress responses
- Most responsive region to ACTH
- Histology: linearly arranged cords of polygonal epithelial cells with abundant eosinophilic cytoplasm and small non-staining vacuoles
Cortex: Zona Reticularis
- Innermost cortical layer
- Primarily produces androgen precursor sex hormones (adrenal androgens)
- Necessary for production of testosterone and estrogen
- Will produce small amounts of glucocorticoids
- Histology: irregular cords of polygonal epithelial cells with small to moderate eosinophilic cytoplasm and few clear cytoplasmic vacuoles
Adrenal Medulla
- Distinguishable from cortex by cellular organization: clusters and irregular trabeculae of chromaffin cells
- Chromaffin cells have moderate granular, lightly basophilic cytoplasm and can appear brown due to staining of granules
- Produces norepinephrine and epinephrine
- Regulation: Controlled by the sympathetic nervous system (SNS)
Production of Adrenal Hormones
- All adrenal hormones are derivatives of cholesterol
- General process:
- Side chain of cholesterol molecule is cleaved off to form pregnenolone
- Step is regulated by ACTH and acts as a rate-limiting step for all adrenocortical hormones
- Hydroxylation reactions modify pregnenolone to create different hormones
- Hormones are not stored in adrenal cells; they are synthesized on demand when secretion is signaled
- All hormones are lipid-soluble and diffuse from cortical cells into the extracellular fluid
- In the bloodstream, they require transport proteins (e.g., corticosteroid-binding globulin)
- Summary formula (representative pathway):
- Cholesterol
ightarrow Pregnenolone - Subsequent hydroxylations yield cortisol, corticosterone, aldosterone, and adrenal androgens
Regulation of Aldosterone
- Primary regulatory pathway:
- Low blood pressure or decreased renal perfusion → juxtaglomerular (JG) cells in the kidneys sense change and secrete renin into the bloodstream
- Renin acts on angiotensinogen (produced by the liver) to form Angiotensin I
- Angiotensin-converting enzyme (ACE) in lung capillaries converts Angiotensin I to Angiotensin II
- Angiotensin II stimulates cells to secrete aldosterone and also causes widespread vasoconstriction (including efferent arterioles in the kidney)
- Representative sequence: ext{Angiotensinogen}
ightarrow ext{Angiotensin I}
ightarrow ext{Angiotensin II}
ightarrow ext{Aldosterone secretion}
- Additional modulator: Atrial natriuretic peptide (ANP)
- ANP is synthesized in atrial cells and released upon atrial stretch due to high blood pressure
- ANP inhibits Na+ reabsorption in the renal collecting ducts; also inhibits parts of the renin–angiotensin–aldosterone system (RAAS)
- Effects include inhibition of renin secretion, inhibition of angiotensin-induced aldosterone secretion, and increased glomerular filtration rate (GFR) → increased Na+ excretion
Regulation of Aldosterone: Additional Details
- ANP effects in renal tubules promote natriuresis and diuresis, contributing to Na+ and water loss when blood pressure is high
Actions of Aldosterone
- Renal effects:
- Stimulates Na+ reabsorption in the ascending limb of the loop of Henle, collecting ducts, and distal renal tubules
- Cl− follows passively to maintain electroneutrality
- Increases secretion of K+ into the tubular lumen
- Mechanism:
- Aldosterone diffuses into target tissue and binds to a nuclear receptor
- Activates transcription/translation of proteins that enhance apical Na+ channels (e.g., ENaC) and basolateral Na+/K+ pumps
- Net effect: Na+ is actively reabsorbed from tubular fluid into the interstitial fluid; water follows passively; K+ is secreted into the lumen
- Regulation of Na+ in blood:
- Aldosterone does not directly regulate Na+ concentration in the blood; this is controlled by osmoreceptors in the hypothalamus which regulate ADH release
Regulation of Cortisol
- Cortisol is the primary adrenal glucocorticoid; corticosterone is produced in smaller amounts (more prominent in amphibians, reptiles, birds, and some rodents)
- Regulation involves the hypothalamic–pituitary–adrenal (HPA) axis:
- Hypothalamus releases ACTH-releasing hormone (ACTH-RH) into the portal system
- ACTH-RH stimulates corticotrophs in the anterior pituitary to secrete ACTH
- ACTH acts on fasciculata cells of the cortex to stimulate cortisol synthesis via a cAMP pathway
- Representative sequence: ext{ACTH-RH}
ightarrow ext{ACTH}
ightarrow ext{cortisol synthesis} - ACTH binding increases adenylyl cyclase activity, raises intracellular cAMP, and drives cortisol production
- Feedback regulation:
- Rising cortisol levels feed back to the hypothalamus and anterior pituitary to decrease ACTH-RH and ACTH release
- Circadian rhythm and stress:
- Cortisol is produced in a circadian pattern with highest levels in the morning and lowest in the evening
- Stress can elevate cortisol production beyond the normal circadian peak
- Chronic stress can lead to hypertrophy of cortisol-producing cells
Regulation of Cortisol: Additional Details
- Cortisol can raise blood glucose levels but is not triggered by hypoglycemia per se
- ACTH and CRH (ACTH-RH) are central to cortisol synthesis; cortisol provides negative feedback to limit further ACTH/CRH release
- Interactions with other hormones (glucagon, epinephrine) help coordinate glucose metabolism during stress
Functions of Cortisol
- Stress response and energy mobilization:
- Stimulates gluconeogenesis and the production of glucose by leveraging amino acids from muscle tissue
- Increases available glucose and maintains energy supply during stress
- Decreases tissue sensitivity to insulin in adipose and lymphoid tissues, reducing glucose uptake from blood
- Promotes lipolysis in adipose tissue, raising circulating free fatty acids
- Stimulates protein catabolism in muscle, raising blood amino acids for gluconeogenesis
- Inhibits DNA synthesis, slowing growth
- Potentiates the effects of glucagon and epinephrine on glucose metabolism
- Immune and inflammatory modulation (high cortisol levels):
- Immunosuppressive effects include inhibition of prostaglandin production, reduced histamine release, decreased phagocytosis and antibody formation, stabilization of granulocyte lysosomal membranes to limit tissue damage, and reduced leukocyte emigration from vasculature
- These actions help dampen prolonged inflammatory responses
Regulation of Androgens
- Adrenal zona reticularis produces androgens such as dehydroepiandrosterone (DHEA) and androstenedione
- Functional notes:
- These adrenal androgens serve as precursors to testosterone and estrogens in peripheral tissues
- They have minimal direct androgenic activity on male sexual characteristics but can be converted to testosterone in other tissues
- In females, adrenal androgens contribute to bone density, muscle mass, and expression of estrous behaviors in some species
- Regulation:
- ACTH stimulates production, but the zona reticularis responds more to androgen-stimulating hormone (from the pituitary) that promotes adrenal androgen production
- ACTH is a primary stimulator, with modulation by other hormonal signals
Any Questions?
- Review the relationships between ACTH, cortisol, aldosterone, and their target tissues
- Understand how changes in blood pressure, electrolyte balance, and stress influence adrenal hormone secretion
- Be able to trace the RAAS pathway and the role of ANP in aldosterone regulation