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Adrenergic vasopressors activate 3 types of receptors: 1) alpha-adrenergic, 2) beta-adrenergic, and 3) dopaminergic. Dopamine is the metabolic precursor of norepinephrine and displays dose-related receptor activity. At infusion rates of less than 5 mcg/kg/minute, dopamine targets dopaminergic receptors. At infusion rates of 5 to 10 mcg/kg/minute, it continues to stimulate dopaminergic receptors but also activates beta-receptors. At high doses, dopamine maintains beta activity while preferentially targeting alpha-receptors. Norepinephrine, the precursor of epinephrine, is much more selective in its targeting of alpha- and beta-receptors than dopamine and has no activity at dopaminergic receptors. Epinephrine is a potent nonselective alpha- and beta-agonist. Its beta effects predominate at lower doses, while alpha1-mediated vasoconstriction predominates at high doses. Phenylephrine is a pure alpha1-agonist, which increases blood pressure via peripheral vasoconstriction.
Non-adrenergic vasopressors include vasopressin and angiotensin II. Vasopressin causes potent peripheral vasoconstriction via vasopressin receptors located on vascular smooth muscle cells. Angiotensin II causes vasoconstriction and increases the release of aldosterone.
Receptor Pharmacology of Vasopressors 
0.5 to 5
5 to 10
10 to 20
0.01 to 0.1
0.1 to 0.2
*Dose listed for dose-related receptor activity only
Locations and Responses of Select Receptors
vascular smooth muscle
positive inotropy and chronotropy
vascular and bronchial smooth muscle
renovascular smooth muscle
Vasoconstrictors can increase myocardial oxygen consumption by increasing ventricular wall tension and decrease myocardial oxygen supply via vasoconstriction of coronary vessels; this can induce myocardial ischemia. Catecholamines can trigger tachyarrhythmias; tachycardia and arrhythmogenesis are more prominent with dopamine than with other vasopressor agents.
Splanchnic hypoperfusion and extensive peripheral vasoconstriction may occur with potent vasoconstrictors.
Catecholamines may have potentially harmful effects on pituitary hormone secretion and immune function; these effects appear to be greatest with dopamine and least with norepinephrine.     
Epinephrine can increase blood glucose and lactate concentrations via stimulation of beta-receptors. 
In general, antihypertensives decrease the response to vasopressors.   Due to their mechanism, angiotensin-converting enzyme (ACE) inhibitors may increase the response to angiotensin II while angiotensin II receptor blockers may decrease the response to angiotensin II. The cardiac effects of dopamine are antagonized by beta-blockers. However, beta-blockers may potentiate the pressor and arrhythmogenic effects of epinephrine. 
Vasodilators (e.g., nitrates, phosphodiesterase inhibitors) antagonize the effects of vasopressors.
Digoxin may potentiate the arrhythmogenic effects of catecholamines.
Halogenated anesthetics increase cardiac autonomic irritability and may sensitize the myocardium to the action of intravenous catecholamines resulting in ventricular arrhythmias.  
Use sympathomimetic vasopressors with caution in patients taking monoamine oxidase inhibitors (MAOIs), including linezolid, due to the risk of severe, prolonged hypertension; reduce the initial vasopressor dose and carefully titrate. In general, do not use sympathomimetic agents concurrently or within 14 days of an MAOI due to an increased risk of hypertensive crisis.      
Use sympathomimetic vasopressors with caution in patients taking tricyclic antidepressants due to the risk of severe, prolonged hypertension.   
Do not use epinephrine to counteract circulatory collapse or hypotension caused by phenothiazines due to a paradoxical further lowering of blood pressure. If a vasoconstrictor is required, norepinephrine and phenylephrine are most suitable.
Never inject intravascular contrast medium after the administration of vasopressors due to potentiation of severe neurologic effects.
Administer vasopressors through a central vein whenever possible; prolonged administration through a peripheral vein may result in extravasation and skin necrosis. If peripheral administration is necessary, use a 20-gauge or larger catheter and assess the site frequently. If extravasation occurs, administer phentolamine 5 to 10 mg directly to the site. 
Correct hypovolemia by restoring blood volume with a suitable plasma expander or whole blood before vasopressor administration. If a vasopressor is continuously administered to maintain blood pressure in the absence of blood volume replacement, severe peripheral and visceral vasoconstriction, decreased renal perfusion and urine output, poor systemic blood flow despite normal blood pressure, tissue hypoxia, and lactic acidosis may occur.  
Patients with a pheochromocytoma may experience a greater sensitivity to the adverse effects of catecholamines. 
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