GTN Mechanism — MFDS Part 1 MCQ
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Correct answer: D — Generating nitric oxide, increasing cGMP and causing predominantly venous vasodilation
GTN is converted at its site of action to nitric oxide, which activates guanylate cyclase and increases intracellular cGMP. This relaxes vascular smooth muscle. Venous capacitance vessels are particularly sensitive, so venodilation increases venous pooling and reduces venous return, ventricular filling and cardiac preload. The resulting reduction in myocardial work and oxygen demand relieves angina. Beta1-adrenoceptor blockade is the mechanism of beta-blockers, while direct L-type calcium-channel blockade describes calcium-channel blockers rather than nitrates. Beta1 stimulation would increase myocardial oxygen demand. Alpha1-mediated vasoconstriction, particularly coronary constriction, is opposite to GTN's vasodilator action. Reflex tachycardia can occur after GTN-induced hypotension, but it is an adverse physiological response rather than its therapeutic mechanism.
Reference: electronic Medicines Compendium. Glyceryl Trinitrate 400 micrograms/metered dose, sublingual spray, Summary of Product Characteristics, section 5.1 Pharmacodynamic properties. Revised 31 March 2023. https://www.medicines.org.uk/emc/product/11759/smpc