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Clinical data
Synonyms Minipress, Vasoflex, Lentopres, Hypovase, others
AHFS/ Monograph
MedlinePlus a682245
License data
Routes of
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability ~60%
Protein binding 97%
Onset of action 30–90 minutes[1]
Elimination half-life 2–3 hours
CAS Number
PubChem CID
ECHA InfoCard 100.038.971 Edit this at Wikidata
Chemical and physical data
Formula C19H21N5O4
Molar mass 383.41 g·mol−1
3D model (JSmol)

Prazosin is a sympatholytic medication that is used to treat high blood pressure, anxiety, and posttraumatic stress disorder (PTSD).[2][3] Prazosin is an α1-blocker that acts as an inverse agonist at alpha-1 adrenergic receptors.[4] These receptors are found on vascular smooth muscle, where they are responsible for the vasoconstrictive action of norepinephrine.[3] They are also found throughout the central nervous system.[5]

As of 2013, prazosin is off-patent in the US, and the FDA has approved at least one generic manufacturer.

Medical use[edit]

Prazosin is orally active and has a minimal effect on cardiac function due to its alpha-1 receptor selectivity. When prazosin is started, however, heart rate and contractility go up in order to maintain the pre-treatment blood pressures because the body has reached homeostasis at its abnormally high blood pressure. The blood pressure lowering effect becomes apparent when prazosin is taken for longer periods of time. The heart rate and contractility go back down over time and blood pressure decreases.

The antihypertensive characteristics of prazosin make it a second-line choice for the treatment of high blood pressure.[6]

Prazosin is also useful in treating urinary hesitancy associated with prostatic hyperplasia, blocking alpha-1 receptors, which control constriction of both the prostate and urethra. Although not a first line choice for either hypertension or prostatic hyperplasia, it is a choice for patients who present with both problems concomitantly.[6]

There is some evidence that this medication is effective in treating nightmares, mixed results in randomized control trials. Prazosin was, however, shown to be more effective when treating nightmares related to PTSD.[7]

The drug is usually recommended for severe stings from Indian Red Scorpion Hottentotta tamulus in Indian Subcontinent.[8][9][10]

Adverse effects[edit]

Common (4–10% frequency) side effects of prazosin include dizziness, headache, drowsiness, lack of energy, weakness, palpitations, and nausea.[2] Less frequent (1–4%) side effects include vomiting, diarrhea, constipation, edema, orthostatic hypotension, dyspnea, syncope, vertigo, depression, nervousness, and rash.[2] A very rare side effect of prazosin is priapism.[2][11] One phenomenon associated with prazosin is known as the "first dose response", in which the side effects of the drug – specifically orthostatic hypotension, dizziness, and drowsiness – are especially pronounced in the first dose.[2]

Orthostatic hypotension and syncope are associated with the body's poor ability to control blood pressure without active alpha-adrenergic receptors. Patients on prazosin should be told to rise to stand up slowly, since their poor baroreflex may cause them to faint if their blood pressure is not adequately maintained during standing. The nasal congestion is due to dilation of vessels in the nasal mucosa.


Prazosin holds promise as a pharmacologic treatment for alcohol dependence after a 2009 pilot trial[12] was completed. A larger controlled Phase II "Clinical Trial of the Adrenergic Alpha-1 Antagonist Prazosin for Alcohol Dependence" was completed in 2018 and published in the American Journal of Psychiatry.[13] While on the surface Prazosin showed an effect greater than placebo, the confidence intervals in the study vastly exceeded the difference, making the data from this study statistically unreliable.[14]

In cancer research, Prazosin triggered apoptosis of glioblastoma‐initiating cells and of their differentiated progeny, inhibited glioblastoma growth in orthotopic xenografts of patient‐derived glioblastoma‐initiating cells, and increased survival of glioblastoma‐bearing mice. Its activity occurred via a PKCδ‐dependent inhibition of the AKT pathway, which resulted in caspase‐3 activation. So, prazosin is a potential anti‐glioblastoma adjuvant drug.[15] Clinical trials will be initiated to confirm these findings. Understanding the mechanism of action of prazosin may pave the way for the development of new potential treatments also for other cancers, since other cancer cells as well display altered PKCδ signaling, including those in colorectal, pancreatic and liver cancer.[16]


  1. ^ Packer M, Meller J, Gorlin R, Herman MV (1979). "Hemodynamic and clinical tachyphylaxis to prazosin-mediated afterload reduction in severe chronic congestive heart failure". Circulation. 59 (3): 531–9. doi:10.1161/01.cir.59.3.531. PMID 761333.
  2. ^ a b c d e "Minipress Prescribing Information" (PDF). United States Food and Drug Administration. Pfizer. February 2015. Retrieved 3 June 2016.
  3. ^ a b "Prazosin: Clinical data". IUPHAR. International Union of Basic and Clinical Pharmacology. Retrieved 3 June 2016. This sympatholytic drug is used in the treatment of hypertension, anxiety and post-traumatic stress disorder. ... Antagonist of alpha-1 adrenoceptors on vascular smooth muscle, thereby inhibiting the vasoconstrictor effect of circulating and locally-released adrenaline and noradrenaline, resulting in peripheral vasodilation.
  4. ^ "Prazosin: Biological activity". IUPHAR. International Union of Basic and Clinical Pharmacology. Retrieved 3 June 2016.
  5. ^ Day, H. E.; Campeau, S.; Watson Jr, S. J.; Akil, H. (1997). "Distribution of alpha 1a-, alpha 1b- and alpha 1d-adrenergic receptor mRNA in the rat brain and spinal cord". Journal of Chemical Neuroanatomy. 13 (2): 115–139. doi:10.1016/S0891-0618(97)00042-2. PMID 9285356.
  6. ^ a b Shen, Howard (2008). Illustrated Pharmacology Memory Cards: PharMnemonics. Minireview. p. 13. ISBN 978-1-59541-101-3.
  7. ^ Kung S, Espinel Z, Lapid MI (2012). "Treatment of nightmares with prazosin: a systematic review". Mayo Clin. Proc. 87 (9): 890–900. doi:10.1016/j.mayocp.2012.05.015. PMC 3538493. PMID 22883741.
  8. ^ Bawaskar, H.S. & P.H. Bawaskar (2008). "Scorpion sting: A study of clinical manifestations and treatment regimes" (PDF). Current Science. 95 (9): 1337–1341. Retrieved 14 April 2010.
  9. ^ Bawaskar, H.S. & P.H. Bawaskar (2007). "Utility of scorpion anti-venin vs. prazosin in the management of severe Mesobuthus tamulus (Indian red scorpion) envenoming at rural settings" (PDF). JAPI. 55: 14–21. Retrieved 14 April 2010.
  10. ^ Pandi, K.; Krishnamurthy, S.; Srinivasaraghavan, R.; Mahadevan, S. (18 February 2014). "Efficacy of scorpion antivenom plus prazosin versus prazosin alone for Mesobuthus tamulus scorpion sting envenomation in children: a randomised controlled trial". Archives of Disease in Childhood. 99 (6): 575–580. doi:10.1136/archdischild-2013-305483. PMID 24550184.
  11. ^ Bhalla AK, Hoffbrand BI, Phatak PS, Reuben SR (October 1979). "Prazosin and priapism". Br Med J. 2 (6197): 1039. doi:10.1136/bmj.2.6197.1039. PMC 1596841. PMID 519276.
  12. ^ Simpson, TL; Saxon, AJ; Meredith, CW; Malte, CA; McBride, B; Ferguson, LC; Gross, CA; Hart, KL; Raskind, M (2009). "A pilot trial of the alpha-1 adrenergic antagonist, prazosin, for alcohol dependence". Alcoholism: Clinical and Experimental Research. 33 (2): 255–63. doi:10.1111/j.1530-0277.2008.00807.x. PMID 18945226.
  13. ^ Study of the Medication Prazosin for Alcohol Dependence
  14. ^ Simpson, Tracy L; Saxon, Andrew J; Stappenbeck, Cynthia; Malte, Carol A; Lyons, Robert; Tell, Dana; Millard, Steven P; Raskind, Murray (2018). "Double-Blind Randomized Clinical Trial of Prazosin for Alcohol Use Disorder". American Journal of Psychiatry: appi.ajp.2018.1. doi:10.1176/appi.ajp.2018.17080913. PMID 30153753.
  15. ^ S. Assad Kahn, S. L. Costa, S. Gholamin, R. T. Nitta, L. G. Dubois, M. Feve, M. Zeniou, P. L. C. Coelho, E. El-Habr, J. Cadusseau, P. Varlet, S. S. Mitra, B. Devaux, M.-C. Kilhoffer, S. H. Cheshier, V. Moura-Neto, J. Haiech, M.-P. Junier, H. Chneiweiss. (2016). The anti-hypertensive drug prazosin inhibits glioblastoma growth via the PKC -dependent inhibition of the AKT pathway. EMBO Molecular Medicine, doi:10.15252/emmm.201505421
  16. ^ Recycling an anti-hypertensive agent to fight brain tumors. ScienceDaily 21 April 2016