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The effects of the sympathetic nervous system can be blocked either by decreasing sympathetic outflow from the brain, suppressing release of norepinephrine from terminals, or by blocking postsynaptic receptors. Adrenergic antagonists reduce the effectiveness of sympathetic nerve stimulation and the effects of exogenously applied agonists, such as isoproterenol. Most often the receptor antagonists are divided into α-receptor antagonists and β-receptor antagonists. This classification will work for us also.


At this point we are finally ready for a short discussion of α2-receptor agonists. Yes, I did write agonists, not antagonists—and in a chapter on antagonists.

α2 Agonists reduce sympathetic nerve activity and are used to treat hypertension.

α2-Receptor activation inhibits both sympathetic output from the brain and release of norepinephrine from nerve terminals. We have already listed one of these drugs—clonidine. There are others: dexmedetomidine, guanabenz, guanfacine, and tizanidine. α-Methyl-dopa is metabolized to α-methylnorepinephrine, which is also an α2 agonist. Because the α2 agonists reduce the output from the brain to the sympathetic nervous system, they have found a use in the treatment of hypertension. Tizanidine has found use in the treatment of spasticity and dexmedetomidine is used for sedation


Many compounds possess some α-blocking activity in addition to their primary action. For example, the antipsychotics have α-antagonist properties. In the case of the antipsychotics, these actions are considered side effects. The drugs that we will consider here have their primary action as α antagonists.

Most of the α antagonists allow vasodilation and, thus, decrease blood pressure.

Remember that α-receptor activation results in vasoconstriction. It should follow that α-receptor blockade will produce vasodilation. This is particularly true when the sympathetic nervous system is firing. For example, the sympathetic nervous system is more active in maintaining blood pressure when a person is standing than when lying down. This is why α-blockade results in a greater decrease in blood pressure in the standing position. This effect is called postural hypotension.

The side effects of the α-blockers are directly related to their α-blocking activity.

For the most part, the side effects of the α-blockers are intuitive. The most common of these effects are postural hypotension and reflex tachycardia.

In Chapter 9, we briefly reviewed the subtypes of α receptors. You could probably have guessed that there are drugs that are specific antagonists for the α1 receptor and others that are specific for the α2 receptor (Figure 10–1). As shown in the figure, phentolamine and tolazoline are about equal in effectiveness at the α1 and α2 receptors, whereas phenoxybenzamine is a much more effective α1- than α2-blocker. The rest of the drugs listed in the figure ...

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