Dopamine is a hormone and neurotransmitter with various effects on the body. When administered as a drug, dopamine causes different effects based on the dosing given. These dose-dependent effects can be divided into a framework of low, medium, and high dose effects.

At low doses, dopamine preferentially activates D1 receptors, which induce vasodilation of renal blood vessels. The major effect of D1 receptor activation by dopamine is an increase in renal blood flow.

At medium doses, dopamine activates beta-1 receptors, which increases cardiac output. This happens by way of increased contractility and increased heart rate.

At high doses, dopamine activates alpha-1 receptors, which cause vasoconstriction of blood vessels. Systemic vasoconstriction increases vascular resistance, which ultimately increases blood pressure. Therefore, the net effect of a high dose of dopamine is an increase in blood pressure.

Key Points

  • Dopamine
    • Sympathomimetic with varying effects at different doses
      • Dopamine sequentially saturates receptors of highest affinity, then binds to receptors with next highest affinity
    • At low doses
      • Mechanism
        • D1 receptor agonist
          • Increases renal perfusion and causes vasodilation
          • D1 stimulation causes vasodilation of most splanchnic beds, including renal, mesenteric, and coronary arteries
        • No D2 receptor effects
          • Given IV, dopamine is too polar to cross BBB, and cannot induce D2 effects
      • Clinical Use
        • Heart failure
          • Natriuresis reduces fluid overload and vasodilation reduces afterload on heart
    • At medium doses
      • Mechanism
        • Beta-1 receptor agonist
          • Increases contractility (inotropy) and HR (chronotropy) to increase cardiac output
      • Clinical Use
        • Heart failure
          • Increases cardiac output, while maintaining renal perfusion
        • Bradycardia
          • 2nd-line after atropine
          • Increase in HR is used to treat unstable bradycardia
    • At high doses
      • Mechanism
        • Alpha-1 receptor agonist
          • Causes vasoconstriction
      • Clinical Use
        • Shock
          • Vasoconstriction increases systemic vascular resistance to increase blood pressure