Epinephrine is a non selective adrenergic agonist and a valuable resuscitative drug because of its effects at multiple adrenergic receptor subtypes. In the treatment of anaphylaxis, epinephrine increases myocardial contractility, accelerates hea rate, causes constriction of vascular smooth muscle, and causes relaxation of bronchial smooth muscle. The principal pharmacologic effects of epinephrine that are beneficial in anaphylaxis are mediated : alpha-1 receptors in vascular smooth muscle, resulting in vasoconstriction, beta-1 receptors in the hea, resulting in increased contractility, and beta-2 receptors in bronchial smooth muscle, resulting in relaxation and relief of bronchoconstriction. (One simple mnemonic for the respective locations of beta1 and beta2 receptors is "one hea, two lungs.") Beta-2 receptors are also found, however, in vascular smooth muscle (especially in skeletal muscle beds), were, just as in bronchial smooth muscle, they promote relaxation. (Epinephrine dilates skeletal muscle vascular beds to maximize oxygen delivery for the "fight-or-flight" response.) The resulting vasodilation in skeletal muscle vascular beds would, by itself, tend to decrease blood pressure, which might tend to worsen the effects of anaphylactic shock, but this effect is mitigated by the intense alpha-1 receptor stimulation, causing vasoconstriction in multiple beds. The principal action of alpha-2 receptors is at the presynaptic nerve terminal, where receptor stimulation reduces the release of norepinephrine from the nerve terminal. Epinephrine does stimulate these receptors, but it does not really contribute to the beneficial actions of epinephrine in resuscitation. Alpha-2 receptors are not located in the hea (except at presynaptic nerve terminals), alpha-2 receptors do not have a significant beneficial effect in resuscitation, and beta-1 receptors are not located in bronchial smooth muscle, but are located in the hea. Beta-1 receptors are located in the hea, not in bronchial smooth muscle. The adrenergic receptor that produces bronchial smooth muscle relaxation is beta-2. Alpha-2 receptors are located primarily at presynaptic nerve terminals, and because the beta-2 receptors in vascular smooth muscle cause vasodilation, this not a helpful effect of epinephrine in this case. Also Know: Epinephrine is indicated for the treatment of anaphylactic reactions and acute asthma exacerbations. It is considered a first-line agent in the treatment of cardiac arrest (i.e., pulseless ventricular tachycardia/ventricular fibrillation, asystole, and pulseless electrical activity). Epinephrine also causes bronchodilation and antagonizes the effects of histamine. Epinephrine significantly increases myocardial oxygen consumption and thus can exacerbate ventricular irritability in the setting of myocardial ischemia. Extravasation causes necrosis and sloughing, and requires prompt infiltration of the affected area with phentolamine. Ref: Miller B.A., Clements E.A. (2011). Chapter 24. Pharmacology of Vasopressor Agents. In J.E. Tintinalli, J.S. Stapczynski, D.M. Cline, O.J. Ma, R.K. Cydulka, G.D. Meckler (Eds), Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e.