RUNNING HEAD: ADRENAL MEDULLA HORMONES
ADRENAL MEDULLA HORMONES
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ADRENAL MEDULLA HORMONES
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Introduction
The current paper is an academic essay on the adrenal medulla as to meet the objections
of understanding the functions and dysfunctions of this organ. Outlined in this essay will be the
various regulatory mechanisms that underpin secretion and the mechanism of action of these
hormones on the target tissues.
Regulation of secretion
The medulla produces primarily the catecholamines epinephrine, norepinephrine and
dopamine (Wong, 2006). Epinephrine is the main catecholamine produced by the adrenal
medulla. These are hormones with varied systemic effects but basically control the “fight or
flight” response in physiological, psychological and environmental stress (Waugh & Grant,
2010).
Control of secretion is through neural mechanisms (De Diego, Gandia, & Garcia, 2008).
The adrenal medulla acts as an amplifier to the sympathetic nervous system and is actually
modified neural tissue composed of neuroendocrine cells hence under similar neural control as
the sympathetic nervous system (De Diego, Gandia, & Garcia, 2008). To illustrate this regulation
the following diagram is used:
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During physiologic, physical or environmental stress for example exercise, fasting, cold
or heat, inflammation, pain, anxiety, hypovolemia, hypoglycemia or emotional stress, the body
perceives a threat to normal homeostatic balance and initiates a response via the hypothalamus
(Barrett, Barman, Boitano, & Brooks, 2009). The hypothalamus mediates this response
depending on the type of stress. Immediate stress will activate the sympathetic nervous system
and the adrenal medulla to produce catecholamines while a prolonged stressor will cause the
release of a corticotropin-releasing hormone that causes the release of ACTH from the anterior
pituitary which in turn activates the adrenal cortex to produce adrenocorticoids (Waugh & Grant,
2010).
A sympathetic nervous discharge will travel through the spinal cord and the sympathetic
preganglionic neuron to synapse with chromaffin cells of the adrenal medulla. The chromaffin
cells act as modified postganglionic neurons and respond to acetylcholine neurotransmitter from
the preganglionic neuron to release mainly epinephrine via exocytosis (De Diego, Gandia, &
Garcia, 2008). The epinephrine is released into circulation to effect the hormonal action on target
organs.
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Mechanism of action at the target organ
Epinephrine has various effects on target organs including increasing the heart rate,
blood pressure, vessel constriction to divert blood from non-essential organs like skin to more
essential organs like heart and brain, increasing the metabolic rate and pupillary dilatation just to
name a few (Waugh & Grant, 2010). These responses are aimed at enhancing and facilitating
recovery from a stressor.
For it to exert its action on any organ, the cells must have cell surface receptors specific
for it. Like most peptide and amine hormones, catecholamines have cell surface receptors.
Catecholamines bind their specific receptors named adrenergic receptors (Badino, Odore, & Re,
2005). They are of two forms: alpha (α) and beta (β). They are further subdivided into α1, α2, β1,
and β2 (Badino, Odore, & Re, 2005). Each of this receptor subtypes have effects on organs,
either inhibitory or excitatory.
The receptors are coupled to membrane proteins that activate an intracellular cascade
leading to release of second messengers that effect cellular action. Beta receptors are coupled to
a G protein that activates adenylyl cyclase on hormone-receptor coupling (Johnson, 2006). This
increases the levels of the second messenger cyclic AMP which will activate protein kinase A.
α1 receptors are coupled to phosphatidylinositol and uses calcium as the second messenger
leading to activation of protein kinase C. α2 are coupled to inhibitory G protein that will decrease
levels of cyclic AMP (Hein, 2006).
The effects of epinephrine on these target organs depends on the subtype of receptors that
the organ expresses. α1 receptors are mostly expressed on smooth muscles and mediate smooth
muscle contraction including vasoconstriction (Hein, 2006). α2 receptors are expressed on
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presynaptic adrenergic nerve terminals and on lipocytes, platelets and some on the smooth
muscle. β1 receptors, on the other hand, are expressed on the heart, lipocytes, kidney, ciliary
body and adrenergic nerve terminals (Tanaka, Horinouchi, & Koike, 2005). Β2 receptors are
postsynaptic on effector cells especially cardiac and smooth muscle (Tanaka, Horinouchi, &
Koike, 2005).
Conclusion
The adrenal medulla produces epinephrine, norepinephrine, and dopamine. This secretion
is mediated by neural control as the chromaffin cell acts as a sympathetic postganglionic neuron
and is under the influence of the sympathetic nervous system. The mechanism of action that
mediates its action on target organs involves the interaction of the hormone with specific
adrenergic cell surface receptors that activate an intracellular cascade and produces its effect
through second messengers cyclic AMP and calcium.
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References
Badino, P., Odore, R., & Re, G. (2005). Are so many adrenergic receptor subtypes really present
in domestic animal tissues? A pharmacological perspective. The Veterinary
Journal, 170(2), 163-174.
Barrett, K. E., Barman, S. M., Boitano, S., & Brooks, H. (2009). Ganong’s review of medical
physiology. 23. NY: McGraw-Hill Medical.
De Diego, A. M. G., Gandia, L., & Garcia, A. G. (2008). A physiological view of the central and
peripheral mechanisms that regulate the release of catecholamines at the adrenal
medulla. Acta physiologica, 192(2), 287-301.
Hein, L. (2006). Adrenoceptors and signal transduction in neurons. Cell and tissue
research, 326(2), 541-551.
Johnson, M. (2006). Molecular mechanisms of β2-adrenergic receptor function, response, and
regulation. Journal of Allergy and Clinical Immunology, 117(1), 18-24.
Tanaka, Y., Horinouchi, T., & Koike, K. (2005). New insights into β‐adrenoceptors in smooth
muscle: distribution of receptor subtypes and molecular mechanisms triggering muscle
relaxation. Clinical and Experimental Pharmacology and Physiology, 32(7), 503-514.
Waugh, A., & Grant, A. (2010). Ross & Wilson Anatomy and Physiology in Health and Illness
E-Book. Elsevier Health Sciences.
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Wong, D. L. (2006). Epinephrine biosynthesis: hormonal and neural control during
stress. Cellular and molecular neurobiology, 26(4-6), 889-898.
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