Norepinephrine activates both α and β receptors, but activates β1 receptors more than β2 receptors. Because of its relatively low affinity for β2 receptors, norepinephrine is not as useful in the treatment of bronchospasm as epinephrine. Why? Because the smooth muscle of the bronchioles are relaxed by activation of β2 receptors.The main effect of α1 stimulation (with an agonist such as phenylephrine) is vasoconstriction.
At low doses, DOPAMINE causes renal and coronary vasodilation. It also activates β1 receptors in the heart.
The indirect-acting sympathomimetic agents act by releasing previously stored norepinephrine.
AMPHETAMINE and its relatives, dexmethylphenidate and methylphenidate, are central nervous system stimulants used to treat attention deficit hyperactivity disorder in children.
Norepinephrine increases total peripheral resistance and mean arterial pressure.
Epinephrine predominantly affects the heart through β1 receptors, causing an increase in heart rate and cardiac output.
Isoproterenol causes a marked decrease in total peripheral resistance and an increase in heart rate and cardiac output.
α2 Agonists reduce sympathetic nerve activity and are used to treat hypertension.
Most of the α antagonists allow vasodilation and, thus, decrease blood pressure.
The side effects of the α-blockers are directly related to their α-blocking activity.
TAMSULOSIN and silodosin are specific antagonists of the α1A receptor and are used in the symptomatic treatment of benign prostatic hypertrophy.
All of the α-blockers are reversible inhibitors of the α receptor, except phenoxybenzamine, which is irreversible.
The β-blockers have widespread use in the management of cardiac arrhythmias, angina, and hypertension.
The adverse effects of these drugs are, for the most part, directly related to their β-blocking abilities.
Some β-blockers are said to have intrinsic sympathomimetic activity. This means they have partial agonist activity, even though they are classified as β-blockers.