Adrenal medulla

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Adrenal medulla
Gray1185.png
Medulla labeled at bottom right.
Gray's p.1280
Artery superior suprarenal artery, middle suprarenal artery, Inferior suprarenal artery
Vein suprarenal veins
Nerve celiac plexus, renal plexus
Lymph lumbar glands
Precursor Neural crest
Anatomical terminology
Medullary part of the adrenal gland (on the pointer).

The adrenal medulla (Latin: medulla glandulae suprarenalis) is part of the adrenal gland. It is located at the center of the gland, being surrounded by the adrenal cortex. It is the innermost part of the adrenal gland, consisting of cells that secrete epinephrine (adrenaline), norepinephrine (noradrenaline), and a small amount of dopamine in response to stimulation by sympathetic preganglionic neurons.

Basic[edit]

The adrenal medulla consists of irregularly shaped cells grouped around blood vessels. These cells are intimately connected with the sympathetic division of the autonomic nervous system (ANS). In fact, these adrenal medullary cells are modified postganglionic neurons, and preganglionic autonomic nerve fibers lead to them directly from the central nervous system. The adrenal medulla therefore affects available energy; heart rate; and metabolism.

Function[edit]

Rather than releasing a neurotransmitter, the cells of the adrenal medulla secrete hormones.

Composed mainly of hormone-producing chromaffin cells, the adrenal medulla is the principal site of the conversion of the amino acid tyrosine into the catecholamines epinephrine, norepinephrine, and dopamine.

Because the ANS, specifically the sympathetic division, exerts direct control over the chromaffin cells the hormone release can occur rather quickly. In response to stressors such as exercise or imminent danger, medullary cells release catecholamines into the blood in a 17:3 ratio of adrenaline to noradrenaline.[1]

Notable effects of adrenaline and noradrenaline include increased heart rate and blood pressure, blood vessel constriction in the skin and gastrointestinal tract, smooth muscle (bronchiole and capillary) dilation, and increased metabolism, all of which are characteristic of the fight-or-flight response. Release of catecholamines is stimulated by nerve impulses, and receptors for catecholamines are widely distributed throughout the body.

Origin[edit]

Medullary cells are derived from the embryonic neural crest and, as such, are simply modified neurons.

In particular, they are modified postganglionic cells of the Autonomic nervous system that have lost their axons and dendrites, receiving innervation from corresponding preganglionic fibers. The cells form clusters around large blood vessels.

Moreover, as the synapses between pre- and postganglionic fibers are called ganglia, the adrenal medulla is actually a ganglion of the sympathetic nervous system.

Pathology[edit]

Neoplasms include:[2]

The adrenal medulla may be poorly formed or absent in cases of absent adrenal gland. The deficiency in circulating catecholamines is mildly symptomatic due to compensation by the autonomous nervous system, except in episodes of hypoglycemia where glycogenolysis cannot be stimulated by circulating epinephrine .[2]

In dopamine beta hydroxylase deficiency, the entire body cannot efficiently produce epinephrine and norepinephrine from dopamine, this results in severe dysautonomia but most crucially due to autonomous nervous system failure which requires epinephrine and norepinephrine as neurotransmitters, dopamine being used in this pathology as an inadequate substitute.[2][3]

See also[edit]

References[edit]

  1. ^ Introduction to Autonomics, Part 2 - Page 5 of 12 anatomy module at med.umich.edu
  2. ^ a b c Fung, M. M.; Viveros, O. H.; O’Connor, D. T. (16 November 2007). "Diseases of the adrenal medulla". Acta Physiologica 192 (2): 325–335. doi:10.1111/j.1748-1716.2007.01809.x. PMC 2576282. PMID 18021328. 
  3. ^ Robertson, D; Haile, V; Perry, SE; Robertson, RM; Phillips JA, 3rd; Biaggioni, I (July 1991). "Dopamine beta-hydroxylase deficiency. A genetic disorder of cardiovascular regulation.". Hypertension 18 (1): 1–8. doi:10.1161/01.hyp.18.1.1. PMID 1677640. 

External links[edit]