The principal pharmacological action of nitroglycerin is relaxation of vascular smooth muscle. Although venous
effects predominate, nitroglycerin produces, in a dose-related manner, dilation of both arterial and venous beds.
Dilation of the postcapillary vessels, including large veins, promotes peripheral pooling of blood, decreases
venous return to the heart, and reduces left ventricular end-diastolic pressure (preload). Nitroglycerin also
produces arteriolar relaxation, thereby reducing peripheral vascular resistance and arterial pressure (after load),
and dilates large epicardial coronary arteries; however, the extent to which this latter effect contributes to the
relief of exertional angina is unclear.
Therapeutic doses of nitroglycerin may reduce systolic, diastolic and mean arterial blood pressure. Effective
coronary perfusion pressure is usually maintained, but can be compromised if blood pressure falls excessively
or increased heart rate decreases diastolic filling time.
Elevated central venous and pulmonary capillary wedge pressures, and pulmonary and systemic vascular
resistance are also reduced by nitroglycerin therapy. Heart rate is usually slightly increased, presumably a reflex
response to the fall in blood pressure. Cardiac index may be increased, decreased, or unchanged. Myocardial
oxygen consumption or demand (as measured by the pressure-rate product, tension-time index, and stroke-work
index) is decreased and a more favorable supply-demand ratio can be achieved. Patients with elevated left
ventricular filling pressure and increased systemic vascular resistance in association with a depressed cardiac
index are likely to experience an improvement in cardiac index. In contrast, when filling pressures and cardiac
index are normal, cardiac index may be slightly reduced following nitroglycerin administration.