L6-Functions of Adrenocortical hormones

corticosteroid

Glucocorticoids:

Mineralocorticoids

Glucocorticoids

cortisol

Mineralocorticoids

aldosterone

Cortisol

steroid hormone; glucocorticoid hormone

Produced in the adrenal gland

Cortisol synthesis

This process begins with the release of CRH from the hypothalamus to go to the corticotropes of the anterior pituitary. Here, it stimulates ACTH release, which then travels to the zona fasciculata of the adrenal cortex.

ACTH binds to melanocortin-2 receptors, which stimulates StAR to bring cholesterol into mitochondria. In the mitochondria, cholesterol is converted to pregnenolone.

In the ER, progesterone goes through more reactions to ultimately become cortisol.

CRH (corticotropin releasing hormone)

It travels to the anterior pituitary gland, where it binds to receptors and stimulates the synthesis and release of adrenocorticotropic hormone (ACTH).

ACTH (adrenocorticotropic hormone)

Stimulates adrenal cortex to release glucocorticoids (cortisol)

Cortisol transport

Corticosteroid-binding globulin (CBG), also known as transcortin.

Binds roughly 80% to 90% of circulating cortisol in the plasma

Only the small fraction of unbound cortisol is biologically active and able to enter cells and exert effects. Bound cortisol is inactive

Corticosteroid-binding globulin (CBG)

utilized in transport of corticosteroid by binding to most of the corticosteroids in circulation

Corisol effects

manages your body's stress response, regulates metabolism, and controls natural daily energy rhythms

cortisol and glucose

to provide your body with fast, ready-to-use energy during stress or fasting.

-Gluconeogenesis

-Reduced Insulin Sensitivity (Cortisol blocks muscle and fat cells from absorbing glucose easily.)

-lower insulin production

cortisol and fat

-Stimulation of Lipolysis

-Increased Free Fatty Acids (FFAs

-Hepatic VLDL Production

- inhibits protein synthesis and decreases peripheral amino acid uptake in muscles

Cortisol and blood pressure

- upregulates epinephrine receptors, making the body more responsive

- causes general vasoconstriction

- causing increased blood pressure (bp)

- has an anti-diuretic effect with sodium retention and potassium loss. mineralocorticoid receptors (MRs)

Cortisol and wound healing

- Suppressed inflammation by lowering pro-inflammatory cytokines

-Reduced Angiogenesis: It blocks the formation of new blood vessels, starving healing tissue of essential oxygen and nutrients

Overall, immune suppression and poor wound healing

cortisol function

-Decreasing bone formation (decreases osteoblast activity)

-Modulation of fetal lung development:

Production of surfactant

-Stimulating cognition and memory

- decreases fibroblast activity (low synthesizing the extracellular matrix (ECM))

Regulation of cortisol

High levels of circulating cortisol act back on the hypothalamus and pituitary gland to suppress further release of CRH and ACTH, preventing excess production

Mineralocorticoids (aldosterone)

Promote reabsorption of Na+ and excretion of K+ in kidneys. Increase blood volume.

produced in the adrenal gland; specifically, in the zona glomerulosa

Aldostrone synthesis

Cholesterol is transported into the mitochondria via the StAR protein. where cholesterol converts into pregnenolone.

Progesterone to Progesterone.

Progesterone to 11-Deoxycorticosterone

11-Deoxycorticosterone to Corticosterone

Corticosterone to Aldosterone

Aldostrone transport

Albumin: Binds about 38% to 60% of circulating aldosterone

Corticosteroid-Binding Globulin (CBG / Transcortin): Binds roughly 22% of circulating aldosterone

Aldostrone Receptor

mineralocorticoid receptor (MR

cytoplasmic MR, the complex translocates into the cell nucleus.

This triggers transcription that increases the expression of epithelial sodium channels

In many target tissues, the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) converts active cortisol into inactive cortisone so that MR is selectively available for aldosterone

Aldostrone and the kidney

Acts on the mineralocorticoid receptors (MR) in the late distal convoluted tubules and collecting ducts of the nephron

Inserts epithelial sodium channels (ENaC) into the cell membrane and boosts sodium-potassium pump activity, moving sodium from the urine back into the bloodstream; increasing blood pressure

Aldosterone and outside the kidney

-Colon (Large Intestine): Promotes sodium and water reabsorption while enhancing potassium excretion

-Salivary Glands: Reduces sodium and chloride loss in saliva while increasing potassium secretion

-Sweat Glands: Minimizes sodium and chloride loss through sweat conservation

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Aldosterone regulation

1. Renin-Angiotensin System (Angiotensin II): When blood pressure, blood volume, or sodium levels drop, the kidneys release the enzyme renin. Renin converts liver-made angiotensinogen into angiotensin II.

2. High Extracellular Potassium (K⁺): Elevated potassium levels directly depolarize adrenal glomerulosa cells, stimulating the synthesis and secretion of aldosterone to promote potassium excretion

3. Adrenocorticotropic Hormone (ACTH): Released by the pituitary gland, ACTH has a stimulatory effect on aldosterone production via the cAMP/PKA pathway