Which statement explains why epinephrine can cause pulmonary vasoconstriction at moderate to high doses?

Which statement explains why epinephrine can cause pulmonary vasoconstriction at moderate to high doses?

• A. Beta2-mediated vasodilation
• B. Endothelial NO release causing vasodilation
• C. Alpha1 stimulation becomes dominant causing pulmonary arterial vasoconstriction
• D. Increased parasympathetic tone

Answer: (C)

Epinephrine acts on both alpha and beta receptors, and its effects depend on dose. At moderate to high doses, alpha1 stimulation becomes dominant in the pulmonary arteries, causing smooth muscle contraction and pulmonary vasoconstriction. The beta2 effect, which would promote dilation, is outrun by the stronger alpha1-mediated constriction at these higher concentrations. This explains why high-dose epinephrine can constrict the pulmonary vasculature. Endothelial NO release would promote dilation, and increased parasympathetic tone isn’t the mechanism by which epinephrine works, so they don’t explain the observed vasoconstriction.

Epinephrine acts on both alpha and beta receptors, and its effects depend on dose. At moderate to high doses, alpha1 stimulation becomes dominant in the pulmonary arteries, causing smooth muscle contraction and pulmonary vasoconstriction. The beta2 effect, which would promote dilation, is outrun by the stronger alpha1-mediated constriction at these higher concentrations. This explains why high-dose epinephrine can constrict the pulmonary vasculature. Endothelial NO release would promote dilation, and increased parasympathetic tone isn’t the mechanism by which epinephrine works, so they don’t explain the observed vasoconstriction.