Prazosin was patented in 1965 and came into medical use in 1974.[8] It is available as ageneric medication.[6] In 2021, it was the 183rd most commonly prescribed medication in the United States, with more than 2million prescriptions.[9][10]
Prazosin is active after taken by mouth and has a minimal effect on cardiac function due to itsα1-adrenergic receptorselectivity. When prazosin is started, however, heart rate and contractility can increase in order to maintain the pre-treatment blood pressures because the body has reachedhomeostasis 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.
Theantihypertensive characteristics of prazosin make it a second-line choice for the treatment of high blood pressure.[11]
Prazosin is also useful in treating urinary hesitancy associated withbenign prostatic hyperplasia, blocking α1-adrenergic receptors, which control constriction of both theprostate andurethra. Although not a first-line choice for either hypertension or benign prostatic hyperplasia, it is a choice for people who present with both problems concomitantly.[11]
During its use for urinary hesitancy in military veterans in the 1990s, Murray A. Raskind and colleagues discovered that prazosin appeared to be effective in reducingnightmares. Subsequent reviews indicate prazosin is effective in improving sleep quality and treating nightmares related topost-traumatic stress disorder (PTSD).[12][13]
Orthostatic hypotension and syncope are associated with the body's poor ability to control blood pressure without active α-adrenergic receptors. The nasal congestion is exacerbated by changing body positions, because α1-adrenergic receptors also control nasal vascular blood flow and alpha blockers inhibit this, in the same way that alpha-adrenergic agonists have the opposite effect of being a decongestant.[22][23]
Prazosin has been said to be the only selective α1-adrenergic receptor antagonist which has been used in the treatment of insomnia to any significant degree.[14] It is used at doses of 1 to 12 mg for this purpose.[14] The combination of prazosin and thebeta blockertimolol may produce greater sedative effects than either of them alone.[15]
Prazosin has been shown to prevent death in animal models ofcytokine storm.[32] As a repurposed drug, prazosin is being investigated for the prevention of cytokine storm syndrome and complications ofCOVID-19 where it is thought to decreasecytokine dysregulation.[33][31][34]
^Reist C, Streja E, Tang CC, Shapiro B, Mintz J, Hollifield M (August 2021). "Prazosin for treatment of post-traumatic stress disorder: a systematic review and meta-analysis".CNS Spectrums.26 (4):338–344.doi:10.1017/S1092852920001121.PMID32362287.S2CID218492349.
^Iwańczuk W, Guźniczak P (2015). "Neurophysiological foundations of sleep, arousal, awareness and consciousness phenomena. Part 1".Anaesthesiol Intensive Ther.47 (2):162–167.doi:10.5603/AIT.2015.0015.PMID25940332.
^Malenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). "Chapter 13: Sleep and Arousal".Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). McGraw-Hill Medical. p. 521.ISBN9780071827706.
^Bawaskar HS, Bawaskar PH (2008). "Scorpion sting: A study of the clinical manifestations and treatment regimes".Current Science.95 (9):1337–1341.JSTOR24103245.
^Pandi K, Krishnamurthy S, Srinivasaraghavan R, Mahadevan S (June 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.PMID24550184.S2CID37215729.
^Riechelmann H, Krause W (1 January 1994). "Autonomic regulation of nasal vessels during changes in body position".European Archives of Oto-Rhino-Laryngology.251 (4):210–213.doi:10.1007/BF00628425.PMID7917253.S2CID24405406.
^"Prazosin: Clinical data".IUPHAR. International Union of Basic and Clinical Pharmacology. Retrieved3 June 2016.
^Day HE, Campeau S, Watson SJ, Akil H (July 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.PMID9285356.S2CID28007564.
^Heijnen CJ, Rouppe van der Voort C, Wulffraat N, van der Net J, Kuis W, Kavelaars A (December 1996). "Functional alpha 1-adrenergic receptors on leukocytes of patients with polyarticular juvenile rheumatoid arthritis".Journal of Neuroimmunology.71 (1–2):223–226.doi:10.1016/s0165-5728(96)00125-7.PMID8982123.S2CID53151786.
