(From Baby Katzung and lecture, 12 Feb 2001, by Brian Buschman)
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Nitrates like nitroglycerine, amyl nitrate and isosorbide-mononitrate act by releasing nitrate groups in smooth muscle, making NO which activates guanylyl cyclase to increase cGMP to relax vascular smooth muscle. These effects cause vasodilatation. They are metabolized very quickly in the liver. Sublingual preparations have a short (10-20 min) duration of action and transdermal ones have a long duration of action (8-12 hours).
Nitrates function by causing venodilation which reduced preload thereby decreasing cardiac work and hence O2 demand. In vasospastic angina it also reduces coronary vasospasm thereby increasing O2 supply.
Adverse effects are those resulting from vasodilatation like reflex tachycardia, orthostatic hypotension and headache from vasodilatation of the meningeal artery.
Nitrates also work in cyanide poisoning. They oxidize the iron of Hb converting it to methemoglobin. Cyanide preferentially binds to methemoglobin. Then you convert the cyanide to thiocynate which is excreted by the kidney. Just be careful not to use too much nitrate because methemoglobin is not able to properly carry O2.
Ca2+-channel blockers like nifedipine, nimodipine, verapamil and diltiazem cause vasodilatation and decreased work of the heart. The baroreceptor reflex can even take this combination and cause reflex tachycardia in response to nifedipine, nimodipine, verapamil and diltiazem.
Clinically they can be used to treat exertional angina by reducing work (O2 demand) and they reduce vasospasm in variant angina.
Verapamil and diltiazem can be used to treat cardiac arrhythmias.
b-Blockers like propranolol have effects that reduce work on the heart. This is effective in the prevention of exertional angina but not unstable or variant angina. They are not good to use for anginal attacks.
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