Why nitroglycerin relieves angina Nitroglycerin has long been used to treat chronic chest pain. Its therapeutic effect arises because it:
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AMimics the action of all signal receptors in the heart
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BIs broken down into peptide hormones that directly stimulate the heart
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CBlocks every chemical cascade that triggers cardiac muscle contraction
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DBreaks down to nitric oxide (NO), which causes vasodilation and increases blood flow to the heart
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EIrreversibly blocks beta-adrenergic receptors to slow the heart rate
Answer
Correct Answer: Breaks down to nitric oxide (NO), which causes vasodilation and increases blood flow to the heart
Explanation
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:
1) Nitroglycerin enters vascular smooth muscle and is enzymatically converted to NO equivalents.2) NO activates soluble guanylyl cyclase → cGMP rises.3) cGMP activates protein kinase G, lowering intracellular Ca2+ and causing relaxation.4) Venodilation reduces cardiac preload; arterial dilation can enhance coronary flow, relieving angina.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