Always in motion is the future.

Week 6: Endocrine/Reproductive

Adrenocortical Hormones

Physiology/Kinesiology

Updated by Tracey 16 August 02

The adrenal glands are at the superior poles of each kidney and consist of two main parts:

Adrenal Medulla: central 20% of the gland, related functionally to sympathetic NS, secreting norepinephrine and epinephrine in response to sympathetic stimulation. Sympathetic system discussed in the nervous system section.
Adrenal Cortex: secretes corticosteroids, synthesized from the sterol cholesterol.
- Mineralocorticoids: affect electrolytes of the ecf's, particularly Na and K. Includes aldosterone (90% of mineralocorticoid activity), desoxycorticosterone, corticosterone.
- Glucocorticoids: increase [blood glucose] with additional affects on protein and fat metabolism. Includes cortisol aka hydrocortisone (95% of glucocorticoid activity), corticosterone.

Mineralocorticoids

Aldosterone causes Na and K transport through the renal tubules, aiding Na absorption and K excretion. Binds with receptor proteins in renal tubules to create enzymes or carrier substances for Na and K transport.

Excess aldosterone -> increased Na and decreased Kin ECF. H₂O is also reabsorbed with Na, -> increased ECF can -> hypertension. K levels of 50% normal (hypokalemia) -> muscle paralysis or weakness.

Lack of aldosterone -> loss of 10-20g Na per day (10-20% in the body) with K conservation. K levels 60-100% above normal (hyperkalemia) can -> cardiac toxicity, including weak contraction or arrhythmia, then cardiac death. Decreased fluid levels -> decreased plasma volume -> circulatory shock and death within 4-8 days.

Secretion regulated by [ECF electrolytes], ECF fluid volume, blood volume, arterial pressure, and other aspects of renal function.

Glucocorticoids

Carbohydrate Metabolism effects include:

Stimulate Gluconeogenesis (formation of glucose from other substances such as protein) by the liver: cortisol increases enzymes required to convert aa's into glucose in liver cells and causes aa's to mobilize from extrahepatic tissues, mainly muscle.
Decrease Glucose Utilization by the Cells: moderate decrease in rate of use.
Elevated [Blood Glucose] -> adrenal diabetes if 50% or more above normal.

Protein Metabolism effects include:

Reduce Cellular Protein: decreased protein synthesis and protein catabolism.
Increase Liver and Plasma Proteins: liver proteins enhanced -> produce plasma proteins -> released into blood
Increased Blood aa's, Diminished aa transport into Extrahepatic Cells: from above factors.

Fat Metabolism effects include:

FA mobilization from adipose tissues -> [plasma ffa] -> increased fat utilization for energy. Important for long-term glucose and glycogen conservation.

Stress -> ACTH (adrenocorticotropic hormone) -> cortisol release (trauma, sympathomimetic substances, forced restraint, disease, etc.) the ffa's and aa's may be readily available for energy or to synthesize other substances.

Cortisol is also an anti-inflammatory...
tissue damage -> release of inflammatory chemicals -> increased blood flow to damaged area -> plasma leakage into damaged areas causing edema -> leukocyte infiltration -> fibrous tissue growth helping healing process
Cortisol believed to stabilize intracellular lysosomal membranes (they don't rupture as easily) -> less inflammatory substances released

ACTH (adrenocorticotropic hormone aka corticotropin or adrenocorticotropin) from the Pituitary regulates cortisol secretion which is in turn controlled by CRF (corticotropin-releasing factor) from the hypothalamus. Pituitary and hypothalamus both work on feedback based on [plama cortisol].

Dysfunction

Hyperadrenalism -- Cushing's Disease: caused by cortisol-secreting tumor in one adrenal cortex or hyperplasia of both from increased ACTH secretion by ant. pituitary. Fat mobilized from lower part of body and deposited in thoracic region. Excess steroid secretion -> edematous appearance of face.

Glucocorticoid excess -> increased [blood glucose] (adrenal diabetes) from excess gluconeogenesis.
Excess protein catabolism (except in liver) -> weakness, suppressed immunity, collagen breakdown in subcutaneous tissues makes them susceptible to tears, osteoporosis due to lack of protein deposition in bones.

Treatment: removal of tumor, or decreasing ACTH secretion (remove tumors in pituitary), last resort adrenalectomy followed by adrenal steroids to replace those not manufactured.