Why nitroglycerin relieves angina Nitroglycerin has long been used to treat chronic chest pain. Its therapeutic effect arises because it:

Introduction:
Angina pectoris results from myocardial ischemia. Nitroglycerin provides rapid symptom relief by expanding vascular capacity and improving coronary perfusion through the nitric oxide pathway.

Given Data / Assumptions:

• Nitroglycerin is a prodrug that can release nitric oxide (NO) in vascular smooth muscle.
• NO stimulates soluble guanylyl cyclase, increasing cGMP.
• cGMP promotes smooth-muscle relaxation and vasodilation.

Concept / Approach:

The therapeutic mechanism hinges on NO-mediated vasodilation, which reduces preload and afterload and can increase coronary blood flow, improving oxygen delivery relative to demand and alleviating ischemic pain.

Step-by-Step Solution:

Verification / Alternative check:

Clinical effects include rapid relief of chest pain and hemodynamic changes consistent with NO-cGMP signaling; tolerance patterns and interactions with PDE-5 inhibitors further corroborate the mechanism.

Why Other Options Are Wrong:

Option A: Nitroglycerin does not mimic receptors; it donates NO.

Option B: It is not converted to peptide hormones.

Option C: It does not shut down all contraction cascades; it relaxes smooth muscle via cGMP.

Option E: It is not a beta-blocker; that is a different drug class.

Common Pitfalls:

Confusing NO donors with beta-blockers or calcium-channel blockers; overlooking the cGMP pathway.

Final Answer:

Breaks down to nitric oxide (NO), which causes vasodilation and increases blood flow to the heart