Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 13.09.2021

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Biogenic hormone belonging to the group of catecholamines and neurotransmitter of the sympathetic nervous system.

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1-3 minutes.

Field of application/use
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Additive to local anaesthetics to reduce their absorption and prolong their effect, for bleeding on the skin and mucous membranes, for various forms of shock and poisoning.

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Limited indication
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Pregnancy, bronchial asthma, cor pulmonale, diabetes mellitus, hypercalcemia, hypokalemia M. Parkinson (increased tremor), severe renal insufficiency. Cave! Sulphite hypersensitivity.

Dosage and method of use
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0.1 μg/kg bw/min as infusion, or 0.3-0.8 mg s.c., or 0.25 mg i.m.

Undesirable effects
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Angina pectoris, cardiac arrhythmia, anaphylaxis (sulfite content of the solution), anxiety, insomnia, danger of cerebral hemorrhage due to abrupt rise in blood pressure, hyperglycemia, hypokalemia, hyperhidrosis.

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See Table 1.

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Narrow-angle glaucoma, pheochromocytoma, prostate hypertrophy, hyperthyroidism, arteriosclerosis, coronary insufficiency, heart muscle damage, absolute arrhythmia, severe hypertension, anaesthesia with inhalation narcotics (cyclopan, halothane), local anaesthesia of the acra (fingers, hands, feet, nose, chin, tongue, etc.).

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The noradrenaline elimination takes place in 2 ways

1. About 8% enters the circulation by diffusion and determines the nordrenlin content in the blood.

2. the remaining 92% are removed from the synaptic cleft by transport. 3 transporters are involved in this biochemical pathway:

  • Noradrenaline transporter (NAT): In the axolemm of the north adrenergic neuron, NAT ensures the reabsorption of noradrenaline into the releasing neuron. Through the cotransport of NACL, energy is used for the active inward flow of noradrenalin. NAT removes about 97% of the released noradrenaline. NAT is of pharmacological interest as a target protein for antidepressants. Nortriptyline is a selective inhibitor of NAT.
  • Extraneuronal Monoamine Transporters (EMT): EMT is a monoaminetransporter located in the plasma membrane of post-synatal and other cells and is responsible for the elimination of about 5% of norepinephrine. For the cations noradreanlin and adrenalin the membrane potential of the cells plays a decisive role.
  • Vesicular monoamine transporters (VMAT-2): VMAT-2 is located in the membrane of the intraneuronal storage vesicles. VMAT-2 ensures that the reabsorbed norepinephrine is stored again. An ATPase in the vesicle membrane ensures high intravescular H+ levels. The energy contained in this gradient is utilized by coupling the inflow of noradrenalin with the H+ efflux. Per absorbed amine molecule 2 hydrogen molecules are expelled. Numerous other amines are substrates for VMAT-2 (dopamine, adrenalin, tyramine, serotonin, histamine, amphetamine, etc.). Reserpine is a selective inhibitor of VMAT-2 and as such causes a depletion of vesicular noradreanlin and adrenalin stores in the CNS.

Degradation of norepinephrine:

Various intracellular enzymes are responsible for the degradation of norepinephrine. They are downstream of the transporters and form a functional unit with them.

1.monoamine oxidase (MAO): The mitochondrial MAO is downstream of the NAT and EMT. It catalyses the oxidative deamination of noradrenalin and normethanephrine to DOPEG (the most important primary metabolite) and MOPEG (see figure). A distinction is made between 2 subtypes of the enzyme:

  • MAO-A: mainly presynaptic occurrence
  • MAO-B: together with MAO-B mainly postsynaptic occurrence

Monoaminooxidase inhibitors (MAO inhibitors) or inhibitors (MAOI) are psychotropic drugs used to treat depression (antidepressants). They exert their effect by blocking monoaminooxidases (MAO), which increases the concentration of monoamines in neurons.

Catechol-O-methyltransferase (COMT): COMT only occurs postsynaptically. The enzyme catalyses, among other things, the important step from DOPEG to MOPEG by transferring a methyl radical. The most important primary metabolite on the postsynaptic side is normetanephrine.

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Norepinephrine interactions


Norepinephrine effect ↓


Reciprocal toxicity ↑, enhanced central effect.

Antidepressants, tricyclic

Blood pressure crisis, avoid combination

Appetite inhibitors

RR increase, reciprocal toxicity ↑.


reciprocal toxicity


noradrenaline effect ↓


Angina pectoris, tachycardia, dihydralazine effect ↓




sympathomimetic effect ↑


RR increase, guanethidine effect ↓


Guanfacine effect ↓


Cardiac arrhythmias

Cardiac glycosides

ventricular arrhythmias




Cardiac arrhythmias




Avoid combination


sympathomimetic effect ↑


High pressure crisis

α -receptor blocker

RR drop, reversal of effect

β -receptor blocker

Blood pressure crisis

Thyroid hormones

Coronary insufficiency

β -sympathomimetics

Reciprocal toxicity ↑


Last updated on: 13.09.2021