|Other names||Fenoldopam mesylate|
|Drug class||Dopamine D1 receptor agonist|
|Main uses||Hypertensive emergencies|
|Side effects||Headache, flushing, nausea, low blood pressure|
|Onset of action||Within 10 min|
|Duration of action||An hour|
|Typical dose||0.01 to 1.6 mcg/kg/min|
|Metabolism||Liver (CYP not involved)|
|Elimination half-life||5 minutes|
|Excretion||Kidney (90%) and fecal (10%)|
|Chemical and physical data|
|Molar mass||305.76 g·mol−1|
|3D model (JSmol)|
Fenoldopam, sold under the brand name Corlopam, is a medication used to treat high blood pressure. Specifically it is used short term for hypertensive emergencies. It is given by continuous injection into a vein. Effects begin within 10 minutes and last for up to an hour.
Common side effects include headache, flushing, nausea, and low blood pressure. Other side effects may include anaphylaxis, palpitations, low potassium, and increased eye pressure. Risk in pregnancy is unclear. It is a dopamine D1 receptor agonist which results in blood vessel dilation. It is a benzazepine derivative.
Fenoldopam is used as an antihypertensive agent postoperatively, and also intravenously (IV) to treat a hypertensive crisis. Since fenoldopam is an intravenous agent with minimal adrenergic effects that improves kidney perfusion, in theory it could be beneficial in people with hypertensive and chronic kidney disease.
In adults for severe blood pressure it is started at 0.01 to 0.3 mcg/kg/minute then increase by 0.05 to 0.1 mcg/kg/minute at 15 minute intervals until desired blood pressure is reached or a max of 1.6 mcg/kg/minute is reached.
Fenoldopam contains sodium metabisulfite, a sulfite that may rarely cause allergic-type reactions including anaphylactic symptoms and asthma in susceptible people. Fenoldopam mesylate administration should be undertaken with caution to patients with glaucoma or raised intraocular pressure as fenoldopam raises intraocular pressure. Concomitant use of fenoldopam with a beta-blocker should be avoided if possible, as unexpected hypotension can result from beta-blocker inhibition of sympathetic-mediated reflex tachycardia in response to fenoldopam.
Fenoldopam causes arterial/arteriolar vasodilation leading to a decrease in blood pressure by activating peripheral D1 receptors. It decreases afterload and also promotes sodium excretion via specific dopamine receptors along the nephron. The renal effect of fenoldopam and dopamine may involve physiological antagonism of the renin-angiotensin system in the kidney. In contrast to dopamine, fenoldopam is a selective D1 receptor agonist with no effect on beta adrenoceptors, although there is evidence that it may have some alpha-1  and alpha-2 adrenoceptor antagonist activity. D1 receptor stimulation activates adenylyl cyclase and raises intracellular cyclic AMP, resulting in vasodilation of most arterial beds, including renal, mesenteric, and coronary arteries. to cause a reduction in systemic vascular resistance. Fenoldopam has a rapid onset of action (4 minutes) and short duration of action (< 10 minutes) and a linear dose–response relationship at usual clinical doses.
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