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Pharmacology · Drugs and Prescriptions

Norepinephrine

Noradrenalini hydrotartras

Norepinephrine (noradrenaline) is a drug identical to the natural mediator of the sympathetic nervous system. It causes pronounced vasoconstriction and a sharp rise in blood pressure, being used primarily in emergency situations for acute hypotension.

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ReceptorsStimulates α1-, α2-, and β1-adrenergic receptors. Has virtually no effect on β2-receptors.
DurationActs for a short time (several minutes). Inactivated by MAO and COMT enzymes.
DangerStrictly contraindicated for subcutaneous and intramuscular administration due to the high risk of necrosis.
Cardiac outputCauses reflex bradycardia, therefore cardiac output does not increase.
How to write a prescription
Rp.: Sol. Noradrenalini hydrotartratis 0,2% - 1 ml
D.t.d. N 10 in amp.
S. Содержимое 2-4 ампул развести в 1000 мл 5% раствора глюкозы; вводить только внутривенно капельно, начиная со скорости 0,1-0,3 мкг/кг/мин

Alternative spellings: Sol. Norepinephrini hydrotartratis 0.2% - 1 ml; Sol. Noradrenalini hydrotartratis 0.2% 1 ml; Sol. Norepinephrini 0.2% - 1 ml

Dosage form
Solution in ampoules 0.2%-1 ml (0.002 g in 1 ml)
Administration
Administer 0.004-0.008 g strictly IV infusion!! Pre-dilute in 1000 ml of 5% glucose solution. Initial dose 0.1-0.3 mcg/kg/min; maximum dose 3-5 mcg/kg/min
Group
Drugs regulating the functions of the peripheral nervous system
4 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Pharmacodynamics and receptor profile

Norepinephrine has a direct stimulating effect on adrenergic receptors, which determines its main pharmacological effects.

  • Effect on blood vessels: Excites $\alpha_1$- and $\alpha_2$-adrenergic receptors, leading to powerful vasospasm of the vascular wall and a rapid increase in blood pressure (BP). Unlike epinephrine (adrenaline), norepinephrine lacks the phase of secondary (subsequent) blood pressure decrease. This is because it practically does not act on $\beta_2$-adrenergic receptors, which are responsible for vasodilation.
  • Effect on the heart: The drug stimulates myocardial $\beta_1$-adrenergic receptors, directly increasing stroke volume and the force of cardiac contractions. However, a sharp jump in BP activates the baroreceptors of the aortic arch. The resulting impulse stimulates the vagus nerve center (n. vagus), leading to an increase in its inhibitory effect on the heart—reflex bradycardia develops (decrease in heart rate). As a result, despite the increase in stroke volume, cardiac output remains unchanged.

Clinical nuance: Reflex bradycardia can be prevented by a pharmacological test—prior administration of an M-cholinergic receptor blocker (e.g., atropine).

Pharmacokinetics and administration guidelines

The only appropriate route for systemic administration of the drug is intravenous (most often as an infusion to maintain a stable therapeutic effect).

  • Oral administration: ineffective, as the substance is completely destroyed in the gastrointestinal tract.
  • Subcutaneous and intramuscular administration: strictly contraindicated. The powerful vasoconstrictive effect causes local arteriolar spasm, leading to ischemia and severe tissue necrosis at the injection site. (In general, the rate of absorption from subcutaneous tissue depends on blood flow. It can be accelerated by massage or the administration of the enzyme hyaluronidase, and slowed down by adding vasoconstrictors. Due to excessive vasoconstriction, noradrenaline itself is not administered subcutaneously).

Biotransformation of norepinephrine occurs via non-microsomal oxidation (oxidative deamination) involving mitochondrial and cytosolic enzymes—monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT). Metabolites, as well as a small fraction of the unchanged substance, are eliminated through the kidneys.

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Clinical application and safety profile

The main indication for prescribing norepinephrine is acute hypotension (conditions accompanied by a critical drop in blood pressure).

Adverse effects:

  • Headache.
  • Respiratory disorders.
  • Heart rhythm disorders (arrhythmias).

Contraindications:

  • Cardiac weakness and atrioventricular block.
  • Severe atherosclerosis.
  • Halothane anesthesia. This inhalational anesthetic dramatically increases myocardial sensitivity (sensitization) to catecholamines, which, against the background of norepinephrine administration, creates an extremely high risk of fatal arrhythmias.

Physiological regulation and reuptake

The release of endogenous noradrenaline into the synaptic cleft is strictly regulated by presynaptic receptors:

  • Stimulation of presynaptic $\alpha_2$-adrenergic receptors inhibits mediator release (negative feedback principle works).
  • Stimulation of presynaptic $\beta$-adrenergic receptors, conversely, increases its release (positive feedback).

After performing its function, the mediator undergoes neuronal reuptake. Pharmacology uses drugs that block this transport mechanism. These include selective inhibitors such as reboxetine (selective blockade) and maprotiline (predominantly blocks noradrenaline reuptake over serotonin, close to tricyclic antidepressants).

There are also mixed-action drugs—serotonin-norepinephrine reuptake inhibitors (SNRIs), for example, venlafaxine. Both the drug itself and its metabolites possess activity. SNRI administration may be accompanied by central nervous system side effects (drowsiness, dizziness) and autonomic disorders (dry mouth, ejaculation problems).

Briefly: answers to topical questions

What are the clinical indications for the use of norepinephrine?

Clinical indications for the use of norepinephrine include conditions accompanied by an acute decrease in blood pressure: acute hypotension, non-ST-segment elevation myocardial infarction complicated by cardiogenic shock, acute decompensated heart failure with cardiogenic shock, as well as generalized meningococcal infection complicated by infectious-toxic shock, to restore blood pressure.

How to memorize

To remember the difference between noradrenaline and adrenaline: "Noradrenaline has NO vasodilation." It does not stimulate vascular $\beta_2$-receptors, so after the pressure spike, there is no phase of its compensatory drop.

Class and exam questions

Why does noradrenaline not increase cardiac output?

Although it directly stimulates cardiac $\beta_1$-receptors and increases stroke volume, the resulting sharp jump in blood pressure causes reflex bradycardia via the vagus nerve. The decrease in heart rate completely neutralizes the increase in stroke volume.

Can noradrenaline be administered intramuscularly?

Strictly prohibited. The drug causes such severe local vascular spasm that blood circulation in this area stops, leading to tissue necrosis.

Which anesthesia is norepinephrine incompatible with?

With halothane. This anesthetic sensitizes the myocardium to catecholamines, which against the background of norepinephrine action can provoke dangerous arrhythmias.

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What else to study on this topic

  • Mechanism of action of norepinephrine reuptake inhibitors (maprotiline, reboxetine).
  • Pharmacology and side effects of SNRIs (venlafaxine).
  • Non-microsomal oxidation of catecholamines: the role of monoamine oxidase (MAO).
  • The role of presynaptic $\alpha_2$- and $\beta$-adrenergic receptors in the regulation of synaptic transmission.
  • Pharmacokinetics of subcutaneous administration and methods of pharmacological modification of absorption.

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