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MECHANISMS OF ANTIANGINAL DRUGS
* Nitrates: The nitrates cause selective smooth muscle relaxa-
tion, probably by release of the nitric oxide (NO) group,
which apparently increases cGMP. There is little direct ef-
fect on myocardial or skeletal muscle. In atherosclerotic
angina, the major therapeutic mechanism is reduction of car-
diac work by peripheral vasodilatation, especially of the
veins. In vasospastic and unstable angina, in which coronary
vasospasm may be a major contributor to the relative ischemia
of the tissue, these drugs may also produce useful coronary
* Beta-adrenoceptor blockers (see Chapter 5): Beta blockers
decrease cardiac work by blocking beta-1 receptors in the
myocardium and thereby decreasing cardiac output. They also
reduce cardiac work by decreasing blood pressure. Although
only 2 members of this group (both nonselective beta block-
ers) have been approved for use in angina at the time of this
writing, all beta-1 selective and nonselective beta blockers
are effective in atherosclerotic angina. These drugs do not
cause vasodilatation. (PgDn key for more text)
* Calcium channel blockers: These agents directly cause
peripheral vasodilatation and directly reduce cardiac work by
reducing influx of activator calcium into smooth muscle and
cardiac cells. In vasospastic and unstable angina, these
drugs may cause a useful degree of coronary vasodilatation.
1. Symposium: Circulation 1985; 72 (Suppl V).
2. Takaro T et al: The Veterans Administration Cooperative
Study of Stable Angina: Current status. Circulation 1982;
65 (Suppl 2): 60.
3. Gersh B J et al: Comparison of coronary artery bypass
surgery and medical therapy in patients 65 years of age or
older. N Engl J Med 1985;313:217.
4. Morse JR, Nesto RW: Double-blind crossover comparison of
antianginal effects of nifedipine and isosorbide dinitrate
in patients with exertional angina receiving propranolol. J
Am Coll Cardiol 1985; 6: 1395.
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