Skeletal formula of noradrenaline
Skeletal formula of propranolol, the first clinically successful beta blocker
Norepinephrine degradation. Metabolizing enzymes are shown in boxes.
Dichloroisoprenaline, the first beta blocker
Norepinephrine (labeled "noradrénaline" in this drawing) processing in a synapse. After release norepinephrine can either be taken up again by the presynaptic terminal, or broken down by enzymes.
Schema of the sympathetic nervous system, showing the sympathetic ganglia and the parts of the body to which they connect.
Brain areas containing noradrenergic neurons.
Chemical structure of octopamine, which serves as the homologue of norepinephrine in many invertebrate species

Beta blockers are competitive antagonists that block the receptor sites for the endogenous catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) on adrenergic beta receptors, of the sympathetic nervous system, which mediates the fight-or-flight response.

- Beta blocker

Beta blockers, which counter some of the effects of noradrenaline by blocking their receptors, are frequently used to treat glaucoma, migraine, and a range of cardiovascular problems.

- Norepinephrine
Skeletal formula of noradrenaline

4 related topics

Alpha

β2 adrenoceptor shown binding carazolol (yellow) on its extracellular site. β2 stimulates cells to increase energy production and utilization. The membrane the receptor is bound to in cells is shown with a gray stripe.

Adrenergic receptor

β2 adrenoceptor shown binding carazolol (yellow) on its extracellular site. β2 stimulates cells to increase energy production and utilization. The membrane the receptor is bound to in cells is shown with a gray stripe.
The mechanism of adrenoreceptors. Adrenaline or noradrenaline are receptor ligands to either α1, α2 or β-adrenoreceptors. α1 couples to Gq, which results in increased intracellular Ca2+ and subsequent smooth muscle contraction. α2, on the other hand, couples to Gi, which causes a decrease in neurotransmitter release, as well as a decrease of cAMP activity resulting in smooth muscle contraction. β receptors couple to Gs, and increases intracellular cAMP activity, resulting in e.g. heart muscle contraction, smooth muscle relaxation and glycogenolysis.

The adrenergic receptors or adrenoceptors are a class of G protein-coupled receptors that are targets of many catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) produced by the body, but also many medications like beta blockers, beta-2 (β2) agonists and alpha-2 (α2) agonists, which are used to treat high blood pressure and asthma, for example.

The biosynthesis of adrenaline involves a series of enzymatic reactions.

Adrenaline

Hormone and medication which is involved in regulating visceral functions .

Hormone and medication which is involved in regulating visceral functions .

The biosynthesis of adrenaline involves a series of enzymatic reactions.

Overall, "Extensive evidence indicates that epinephrine (EPI) modulates memory consolidation for emotionally arousing tasks in animals and human subjects.” Studies have also found that recognition memory involving adrenaline depends on a mechanism that depends on β adrenoceptors. Adrenaline does not readily cross the blood–brain barrier, so its effects on memory consolidation are at least partly initiated by β adrenoceptors in the periphery. Studies have found that sotalol, a β adrenoceptor antagonist that also does not readily enter the brain, blocks the enhancing effects of peripherally administered adrenaline on memory. These findings suggest that β adrenoceptors are necessary for adrenaline to have an effect on memory consolidation.

Dopamine is then converted to noradrenaline by dopamine beta-hydroxylase which utilizes ascorbic acid (vitamin C) and copper.

Visual definition of an antagonist, where it compared to agonists and reverse agonists.

Phentolamine

Reversible nonselective α-adrenergic antagonist.

Reversible nonselective α-adrenergic antagonist.

Visual definition of an antagonist, where it compared to agonists and reverse agonists.

This hypotension is sensed by the baroreceptor reflex, which results in increased sympathetic nerve firing on the heart, releasing norepinephrine.

It also has usefulness in the treatment of cocaine-induced cardiovascular complications, where one would generally avoid β-blockers (e.g. metoprolol), as they can cause unopposed α-adrenergic mediated coronary vasoconstriction, worsening myocardial ischemia and hypertension.

Normal remnant adrenal gland (left) with a pheochromocytoma (right) involving the adrenal medulla

Pheochromocytoma

Closely related to, but not to be confused with Paraganglioma

Closely related to, but not to be confused with Paraganglioma

Normal remnant adrenal gland (left) with a pheochromocytoma (right) involving the adrenal medulla
Adrenal gland; the medulla (center, red) is the origin of the adrenal gland
There are two adrenal glands, highlighted in yellow, on top of each of the kidneys
Structure of epinephrine
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FDG PET – the tumor is appreciated as the dark structure in the patient's left chest. Darkened structures at head of patient is brain, in the abdomen are the kidneys, in the pelvis is the bladder. These are normal.
Histopathology on the resected tumor confirms the diagnosis, by typical features as shown.
Patient receiving radiation therapy to the region of the head and neck. Full facial mold is in-place to protect areas where they do not want exposure
Top: Purple lesions are metastatic disease detected with DOTATATE imaging. Bottom: Same patient. Purple lesions are metastatic disease detected with FDG PET
Likelihood of diagnosis when an adrenal-nodule is identified; pheochromocytoma is in yellow near the top-right corner
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The Zebra has become a powerful symbol in the pheochromocytoma advocacy community and represents the rare medical cases that are more likely to be misdiagnosed

3) Toxic Myocarditis: Even in patients without myocardial damage, excessive catecholamines can result in abnormal ST changes on an ECG. Norepinephrine (a catecholamine) is hypothesized to result in damaged cardiac tissue by inhibiting coronary blood flow and depriving cells of oxygen, thus resulting in ischemic tissue. Fortunately, following tumor excision and the subsequent quelling of catecholamines, the damage has been proven reversible.

2) Pharmaceutical Interference: Many prescription, over-the-counter, and illicit substances can interfere with the proper collection of plasma metanephrines and lead to false-positive results. Providers should review a patient's medication list in-detail and have a discussion if temporarily discontinuing any of the interfering medications is possible. The most reported medications to result in falsely elevated metanephrines include: β-adrenoceptor blockers, phenoxybenzamine, tricyclic antidepressants, monoamine oxidase inhibitors, serotonin norepinephrine reuptake inhibitors (SNRI), and methyldopa. As the majority of these medications are commonly prescribed for psychiatric conditions, a conversation with the prescriber may be necessary to facilitate alternative therapeutic options while the patient is undergoing evaluation for a pheochromocytoma. After any possible prescription medications have been held, it is important to review any over-the-counter medications/supplements as well as the commonly used acetaminophen and pseudoephedrine cause false elevations in metanephrine levels. Finally, it is important to have open, non-judgemental discussions about the patient's recreational substance use. Amphetamines, nicotine, and cocaine can result in marked plasma norepinephrine levels.