Cocaine-induced vasoconstriction is best described as which of the following?

Cocaine-induced vasoconstriction is best described as which of the following?

• A. Direct vasodilation
• B. Inhibits epinephrine release
• C. Enhances prostaglandin synthesis
• D. Potentiates norepinephrine effect

Answer: (D)

Cocaine-induced vasoconstriction occurs because cocaine blocks the reuptake of norepinephrine at sympathetic nerve endings, leaving more norepinephrine in the synaptic cleft to activate alpha-adrenergic receptors on vascular smooth muscle. This boosts sympathetic signaling, increases intracellular calcium in the smooth muscle, and causes sustained narrowing of vessels. The result is heightened vascular tone, potential hypertension, and risk of ischemia. Direct vasodilation wouldn’t produce constriction, so that option doesn’t fit. Cocaine’s main effect isn’t inhibiting epinephrine release; it increases norepinephrine effects by preventing reuptake. Prostaglandin synthesis isn’t the primary mechanism for cocaine’s vasoconstriction, so that choice isn’t correct either.

Cocaine-induced vasoconstriction occurs because cocaine blocks the reuptake of norepinephrine at sympathetic nerve endings, leaving more norepinephrine in the synaptic cleft to activate alpha-adrenergic receptors on vascular smooth muscle. This boosts sympathetic signaling, increases intracellular calcium in the smooth muscle, and causes sustained narrowing of vessels. The result is heightened vascular tone, potential hypertension, and risk of ischemia.

Direct vasodilation wouldn’t produce constriction, so that option doesn’t fit. Cocaine’s main effect isn’t inhibiting epinephrine release; it increases norepinephrine effects by preventing reuptake. Prostaglandin synthesis isn’t the primary mechanism for cocaine’s vasoconstriction, so that choice isn’t correct either.