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indicationPhenylephrine is mainly used to treat nasal congestion, but may also be useful in treating hypotension and shock, hypotension during spinal anaesthesia, prolongation of spinal anaesthesia, paroxysmal supraventricular tachycardia, symptomatic relief of external or internal hemorrhoids, and to increase blood pressure as an aid in the diagnosis of heart murmurs.
pharmacologyPhenylephrine is a powerful vasoconstrictor. It is used as a nasal decongestant and cardiotonic agent. Phenylephrine is a postsynaptic α1-receptor agonist with little effect on β-receptors of the heart. Parenteral administration of phenylephrine causes a rise in systolic and diastolic pressures, a slight decrease in cardiac output, and a considerable increase in peripheral resistance; most vascular beds are constricted, and renal, splanchnic, cutaneous, and limb blood flows are reduced while coronary blood flow is increased. Phenelephrine also causes pulmonary vessel constriction and subsequent increase in pulmonary arterial pressure. Vasoconstriction in the mucosa of the respiratory tract leads to decreased edema and increased drainage of sinus cavities.
mechanism of actionIn general, α1-adrenergic receptors mediate contraction and hypertrophic growth of smooth muscle cells. α1-receptors are 7-transmembrane domain receptors coupled to G proteins, Gq/11. Three α1-receptor subtypes, which share approximately 75% homology in their transmembrane domains, have been identified: α1A (chromosome 8), α1B (chromosome 5), and α1D (chromosome 20). Phenylephrine appears to act similarly on all three receptor subtypes. All three receptor subtypes appear to be involved in maintaining vascular tone. The α1A-receptor maintains basal vascular tone while the α1B-receptor mediates the vasocontrictory effects of exogenous α1-agonists. Activation of the α1-receptor activates Gq-proteins, which results in intracellular stimulation of phospholipases C, A2, and D. This results in mobilization of Ca2+ from intracellular stores, activation of mitogen-activated kinase and PI3 kinase pathways and subsequent vasoconstriction. Phenylephrine produces its local and systemic actions by acting on α1-adrenergic receptors peripheral vascular smooth muscle. Stimulation of the α1-adrenergic receptors results in contraction arteriolar smooth muscle in the periphery. Phenylephrine decreases nasal congestion by acting on α1-adrenergic receptors in the arterioles of the nasal mucosa to produce constriction; this leads to decreased edema and increased drainage of the sinus cavities.
biotransformationUndergoes extensive first-pass metabolism in the intestinal wall and extensive metabolism in the liver. Sulfate conjugation, primarily in the intestinal wall, and oxidative metabolism by monoamine oxidase (MAO) represent the principle routes of metabolism. Glucuronidation occurs to a lesser extent. Phenylephrine and its metabolites are mainly excreted in urine/ .
absorptionCompletely absorbed after oral administration. It has a reduced bioavailability (compared to pseudoephedrine) following oral administration due to significant first-pass metabolism in the intestinal wall. Compared to IV administration, bioavailability is approximately 38%. Peak serum concentrations are achieved approximately 0.75-2 hours following oral administration. Phenylephrine should be administered parenterally to achieve cardiovascular effects. Occasionally, systemic effects are observed following oral inhalation.
half life2.1 to 3.4 hours
drug interactionsAlseroxylon: Increased arterial pressure
Amitriptyline: The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of phenylephrine.
Amoxapine: The tricyclic antidepressant, amoxapine, increases the sympathomimetic effect of phenylephrine.
Clomipramine: The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of phenylephrine.
Deserpidine: Increased arterial pressure
Desipramine: The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of phenylephrine.
Doxepin: The tricyclic antidepressant, doxepin, increases the sympathomimetic effect of phenylephrine.
Ergonovine: Possible marked increase of arterial pressure
Guanethidine: Phenylephrine may decrease the effect of guanethidine.
Imipramine: The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of phenylephrine.
Isocarboxazid: Increased arterial pressure
Linezolid: Possible increase of arterial pressure
Methyldopa: Increased arterial pressure
Methylergonovine: Possible marked increase of arterial pressure
Midodrine: Increased arterial pressure
Moclobemide: Moclobemide increases the sympathomimetic effect of phenylephrine.
Nortriptyline: The tricyclic antidepressant, nortriptyline, increases the sympathomimetic effect of phenylephrine.
Oxytocin: Possible marked increase of arterial pressure
Pargyline: Increased arterial pressure
Phenelzine: Increased arterial pressure
Protriptyline: The tricyclic antidepressant, protriptyline, increases the sympathomimetic effect of phenylephrine.
Rasagiline: Increased arterial pressure
Reserpine: Increased arterial pressure
Tranylcypromine: The MAO inhibitor, Tranylcypromine, may increase the vasopressor effect of the alpha1-agonist, Phenylephrine. Concomitant therapy should be avoided.
Trimipramine: Trimipramine may increase the vasopressor effect of the alpha1-agonist, Phenylephrine. Avoid combination if possible. Monitor sympathetic response to therapy if used concomitantly.