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Norepinephrine is less beta2 adrenomimetic than epinephrine so more selective so less bronchospasm so may be therofore better in treatment of cardiac failure and different shocks.

However, I am not sure.

I have some intuition that some of them is somehow analog of the other one.

PubMed about norepinephrine in Pharmacology

  • Sympathomimetics
  • Adrenergic alpha-Agonists
  • Vasoconstrictor Agents

PubMed about epinephrine in Pharmacology

  • Bronchodilator Agents (beta2)
  • Mydriatics (beta2)
  • Adrenergic alpha-Agonists
  • Sympathomimetics
  • Adrenergic beta-Agonists (this causes those two first indications)
  • Vasoconstrictor Agents

which is logical because epinephrine is nonselective beta2. However, I am not sure if those properties include all accepted indications.

This proposes me that norepinephrine can be used better in acute situations. However, I know that epinephrine injections are more given to allergic people to carry for anaphylactic shock. Why so? Probably, because of price. How does the indications of norepinephrine differ from those in epinephrine?

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  • $\begingroup$ You're proposing several problems: cardiogenic/septic shock, bronchospasm, and anaphyllaxix. Cost isn't the factor. Epinephrine is the drug of choice for anaphyllaxis because it decreases edema through its alpha-1 adrenergic vasoconstrictor effects on the small arterioles and precapillary sphincters in most body organ systems. If blood pressure were the major consideration, another agent would be used. Dobutamine is used for cardiogenic shock because it is also a positive inotrope. You can't pick two drugs and ask how they differ (too broad) without the effect (indication?) you're looking for. $\endgroup$ – anongoodnurse Dec 4 '14 at 14:01
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The differences in the action/indication is because of differential affinity of the two molecules to different adrenergic receptors. The wikipedia page on Ardenergic receptor has a table which summarizes this.

Wikipedia doesn't cite references for it. You may have a look at some of the following old articles.

  • α- and β-Adrenergic Receptor Subtypes

    In the periphery, α1-receptors are located postsynaptically, mediating the excitatory effects of catecholamines at α-receptors. α2-Adrenoceptors, on the other hand, are autoreceptors involved in the regulation of noradrenaline (norepinephrine) release. In the central nervous system, both α1- and α2-receptors exist on postsynaptic cells; there are also 2 principal subtypes of β-adrenoceptors. β1-Receptors have a high affinity for both noradrenaline and adrenaline (epinephrine) and are found in the heart, brain, and adipose tissue. β2-Receptors have a low affinity for noradrenaline and are involved in mediation of relaxation of vascular and other smooth muscles and in many of the metabolic effects of catecholamines.

  • β-Adrenergic Receptor Subtypes: Properties, Distribution, and Regulation

             enter image description here

                  NE=Norepinephrine, EPI=Epinephrine, ISO=Isoprenaline

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  • $\begingroup$ NE properties seem to go little over each other: its alphanergic properties cancel out some of its betanergic properties. This may result in the fact that epinephrine is more potent drug than norepinephrine. At least, it is used more widely and has more indications including PCR and acute anaphylaxis, in contrast to norepinephrine. I wonder if there are any indications of norepinephrine where you cannot use epinephrine. Probably, one such a property is acute hypotension. Probably some stability issue with the epinephrine or something. $\endgroup$ – Léo Léopold Hertz 준영 Dec 4 '14 at 12:46
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    $\begingroup$ @Masi α-receptor mediated responses would be more responsive to NE; I don't think it will cancel out. α-receptor mediated responses are synaptic. Very localized and not endocrine....... I don't think there is a stability issue. NE is specifically administered for acute hypotension. There are other synthetic agonists that target only one type of receptor like salbutamol. $\endgroup$ – WYSIWYG Dec 4 '14 at 12:54

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