Cocaine vasoconstriction mechanism?

Cocaine vasoconstriction mechanism?

• A. Blocks calcium channels
• B. Potentiates norepinephrine
• C. Increases histamine release
• D. Activates alpha-adrenergic receptors

Answer: (B)

Cocaine causes vasoconstriction mainly by increasing norepinephrine signaling. It blocks the reuptake of norepinephrine into sympathetic nerve endings, so more NE remains in the synaptic space. This elevated NE then stimulates alpha-1 adrenergic receptors on vascular smooth muscle, causing contraction and vasoconstriction. This is an indirect mechanism—the drug doesn’t directly activate the receptors but enhances the body's own signaling by NE. The other ideas don’t fit as well: blocking calcium channels isn’t the primary driver of cocaine-induced vasoconstriction; histamine release isn’t the main mechanism in this context; and cocaine doesn’t directly activate alpha receptors—it increases NE, which then acts on those receptors.

Cocaine causes vasoconstriction mainly by increasing norepinephrine signaling. It blocks the reuptake of norepinephrine into sympathetic nerve endings, so more NE remains in the synaptic space. This elevated NE then stimulates alpha-1 adrenergic receptors on vascular smooth muscle, causing contraction and vasoconstriction. This is an indirect mechanism—the drug doesn’t directly activate the receptors but enhances the body's own signaling by NE. The other ideas don’t fit as well: blocking calcium channels isn’t the primary driver of cocaine-induced vasoconstriction; histamine release isn’t the main mechanism in this context; and cocaine doesn’t directly activate alpha receptors—it increases NE, which then acts on those receptors.