Adrenergic drugs are medications that stimulate or inhibit adrenergic receptors. Adrenergic receptors mediate the action of noradrenaline, also known as norepinephrine, and adrenaline, also known as epinephrine. Adrenergic neurotransmission is responsible for the body’s sympathetic response - the “fight or flight” state - which dilates pupils, increases heart rate and respiratory rate, diverts blood flow to the muscles, inhibits activities that are not essential in an emergency, and releases stored energy. Adrenergic receptors are also active in the central nervous system, in processes such as memory and alertness. There are several types of adrenergic receptors, all of which are G-protein coupled, but they differ in several aspects: - They couple with different G-proteins, leading to different downstream signalings, and hence different cellular responses. - They differ in sensitivity to different drugs.

- While several receptors may coexist in the same tissue, there is usually one that predominates and is mainly responsible for the tissue’s adrenergic response. For example, the alpha-1 receptor predominates in peripheral vascular smooth muscle; its activation induces vasoconstriction. The beta-1 receptor is prominent in the heart; it increases heart rate and cardiac contractility when activated. Beta-2 activation results in bronchodilation in the lungs, and alpha-2 reduces sympathetic outflow in the brainstem. Alpha-2 can also act at the pre-synaptic neuron, where it inhibits neurotransmitter release as a feedback mechanism. Most adrenergic drugs act directly at the receptors; only a few act indirectly by promoting neurotransmitter release or by preventing its degradation. Non-specific drugs are those that can bind to several receptors. Non-specific agonists include epinephrine, norepinephrine, and dopamine. Their relative activity via different receptors depends on the dose administered.

For example, epinephrine has a greater affinity for beta receptors in small doses, but can bind to alpha receptors equally well at higher doses. At low levels, epinephrine preferentially binds to vascular beta-2-receptors and causes vasodilation. As the concentration of epinephrine increases, lower affinity alpha-receptors begin to bind epinephrine, producing vasoconstriction. Because there are more alpha-receptors than beta-receptors in peripheral blood vessels, alpha-mediated vasoconstriction eventually overrides beta-mediated vasodilation. Thus, at higher pharmacologic doses, epinephrine induces vasoconstriction via alpha receptors; increases heart rate, cardiac contractility via beta-1 receptor; and dilates bronchi via beta-2 receptor. Epinephrine is the treatment of choice for cardiac arrest, anaphylaxis, and severe croup. Specific drugs target only a certain type of receptor:

- Alpha-1 specific agonists induce smooth muscle contraction and are used as vasopressors for treatment of shock, hypotension; as nasal decongestants; or to dilate pupils. Alpha-1 antagonists, on the other hand, are used to treat hypertension, and to relax smooth muscle within the prostate for treatment of benign prostatic hyperplasia. - Alpha-2 agonists act on alpha-2 receptors in the brainstem to reduce sympathetic tone, and are used to treat hypertension. Stimulation of peripheral alpha-2 receptors may initially cause vasoconstriction, but it is quickly overridden by the central effect. - Beta-1 agonists increase heart rate and contractility, and are indicated for treatment of cardiogenic shock and heart failure. - Beta-2 agonists relax smooth muscles. They are used to dilate bronchi, for treatment of asthma, obstructive pulmonary disease, and anaphylaxis.

Some are used to relax uterine smooth muscle to delay preterm birth. Beta antagonists, or beta blockers, are used for the treatment of hypertension, ischemic heart disease, obstructive cardiomyopathy, and arrhythmias.

Adrenergic Drugs - Pharmacology, Animation

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Adrenergic Drugs - Pharmacology, Animation

Adrenergic Drugs - Pharmacology, Animation

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