Medicine & USMLE


Sympathomimetics and Sympatholytics (Old)
  1. Dopamine
  2. Fenoldopam
  3. Dobutamine
  4. Epinephrine
  5. Norepinephrine
  6. Isoproterenol
  7. Midodrine
  8. Phenylephrine and Pseudoephedrine
  9. (Alpha) Methyldopa
  10. Clonidine (and Guanfacine)
  11. Tizanidine


Norepinephrine is a sympathetic agonist or activator at alpha-1 and beta 1 receptors, with predominant effects at alpha 1 receptors. Alpha-1 receptor activation causes vasoconstriction of blood vessels, which can increase vascular resistance and blood pressure. This increase in blood pressure makes norepinephrine useful for treating hypotension or extremely low blood pressures, such as in the setting of shock. Adverse effects include a compensatory slowing of the heart, known as reflex bradycardia. Also, local blood vessel constriction around the injection site or norepinephrine can lead to local tissue necrosis, which is prevented by local co-injections of small doses of alpha-1 blockers like phentolamine.

Key Points

  • Norepinephrine
    • Pharmacologic form of endogenous norepinephrine (NE)
      • NE normally secreted by adrenal medulla to induce sympathetic nervous system activity
    • Mechanism
      • Strong Alpha-1 Receptor Agonist
        • Act on blood vessels to induce vasoconstriction
          • Increases vascular resistance and increased blood pressure
      • Weak Beta-1 Receptor agonist
        • Acts on heart to induce modest increase in myocardial contractility and heart rate
      • Weak Alpha-2 Receptor agonist
        • Alpha-2 receptors are centrally located and cause weak inhibition of the sympathetic system; this effect is made negligible by strong alpha-1 agonism
    • Clinical Use
      • Treats Hypotension/Septic Shock
        • Mainly via Alpha-1 effects
    • Adverse Effects
      • Reflex bradycardia
        • Increased BP due to vasoconstriction causes compensatory decrease in heart rate
      • Local tissue necrosis at injection site
        • Due to local alpha-1 mediated vasoconstriction in blood vessels
        • Prevented by local injection of an alpha-1 blocking drug, such as phentolamine