In 1857, the eminent physician T. Lauder Brunton of Edinburgh administered amyl nitrate a known vasodepressic, by inhalation and noted that anginal pain was relieved within 30-60 seconds. The action of amyl nitrate was transitory however and the dosage was difficult to adjust. Subsequently, William Murrell decided that the action of nitroglycerin mimicked that of amyl nitrate, and he established the use of sublingual nitroglycerin for relief of the acute anginal attack and as a prophylactic agent to be taken prior to exertion. The cardiovascular effects of nitrates include relaxation of the smooth muscle in arteries and veins. Nitrates appear to cause a redistribution of blood flow in the heart when the coronary circulation is partially occluded.
Nitrates can also reduce myocardial oxygen demand.
The major determinants of myocardial oxygen consumption include left ventricular wall tension, heart rate, and contractility of the myocardium. Ventricular wall tension is affected by a number of factors that may be considered under the categoies of preload and afterload . Nitrates are preload reducers because the decrease venous return to the heart thus decresing end-diastolic ventricular volume, thereby decreasing oxygen consumption. Nitrates are afterload reducers because they exhibit a reduction in resistance against which the ventricle must eject. This reduces peripheral resistance and myocardial work, thus reducing oxygen consumption.