Why the study?
What is the mechanism of action of nitroglycerin in relieving angina pectoris in patients with coronary heart disease?
What is the mechanism of action of nitroglycerin in relieving angina pectoris in patients with coronary heart disease?
Discusses the potential mechanisms of action of nitroglycerin in relieving angina pectoris, suggesting it may act through reduction of cardiac work rather than direct coronary vasodilation.
Challenges direct coronary vasodilation as nitroglycerin’s primary mechanism; leaves open reduced cardiac work for prospective validation.
The usefulness of nitroglycerin (glyceryl trinitrate) in relieving angina pectoris is undisputed: it has one of the clearest pharmacological effects in man. However, the mechanism of its action is not well understood In animal experiments the nitrites cause relaxation of smooth muscle, notably in the vessels, and an increased coronary flow can easily be demonstrated However, it is doubtful whether nitroglycerin relieves angina pectoris by dilatation of the coronary arteries. In the first place, ischemia by itself provides a very powerful vasodilator stimulus due to the accumulation of vasodilating substances in the anoxic tissue, so that it is unlikely that artificial vasodilator agents can act upon vessels already under a maximal influence of endogenous metabolites. An action of nitroglycerin on the larger arterio- sclerotic coronary arteries also seems unlikely. Another mechanism of action of nitrites may be through reduction of the work of the heart. Brunton (1867) pointed out that amyl nitrite diminished the tension of the pulse, and it has also been found that the cardiac output at rest is decreased after nitroglycerin
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Christensson et al. (1965) studied this question.
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