Prazosin

Prazosin is an alpha-adrenergic blocker and is a sympatholytic drug used to treat high blood pressure and anxiety, PTSD, and panic disorder.

The effects of voluntary exercise and prazosin on capillary rarefaction and metabolism in streptozotocin-induced diabetic male rats.[Pubmed:27932675]

J Appl Physiol (1985). 2017 Mar 1;122(3):492-502.

Type-1 diabetes mellitus (T1D) causes impairments within the skeletal muscle microvasculature. Both regular exercise and Prazosin have been shown to improve skeletal muscle capillarization and metabolism in healthy rats through distinct angiogenic mechanisms. The aim of this study was to evaluate the independent and additive effects of voluntary exercise and Prazosin treatment on capillary-to-fiber ratio (C:F) in streptozotocin (STZ)-treated diabetic rats. STZ (65 mg/kg) was intraperitoneally administered to male Sprague-Dawley rats (n = 36) to induce diabetes, with healthy, nondiabetic, sedentary rats (n = 10) as controls. The STZ-treated rats were then divided into sedentary (SED) or exercising (EX; 24-h access to running wheels) groups and then further subdivided into Prazosin (Praz) or water (H2O) treatment groups: nondiabetic-SED-H2O, STZ-SED-H2O, STZ-EX-H2O, STZ-SED-Praz, and STZ-EX-Praz. After 3 wk, untreated diabetes significantly reduced the C:F in tibialis anterior (TA) and soleus muscles in the STZ-SED-H2O animals (both P < 0.05). Voluntary exercise and Prazosin treatment independently resulted in a normalization of C:F within the TA (1.86 +/- 0.12 and 2.04 +/- 0.03 vs 1.71 +/- 0.09, P < 0.05) and the soleus (2.36 +/- 0.07 and 2.68 +/- 0.14 vs 2.13 +/- 0.12, P < 0.05). The combined STZ-EX-Praz group resulted in the highest C:F within the TA (2.26 +/- 0.07, P < 0.05). Voluntary exercise volume was negatively correlated with fed blood glucose levels (r(2) = -0.7015, P < 0.01) and, when combined with Prazosin, caused further enhanced nonfasted glucose (P < 0.01). Exercise and Prazosin reduced circulating nonesterified fatty acids more than either stimulus alone (P < 0.05). These results suggest that the distinct stimulation of angiogenesis, with both regular exercise and Prazosin treatment, causes a cooperative improvement in the microvascular complications associated with T1D.NEW & NOTEWORTHY It is currently well established that poorly controlled diabetes reduces both skeletal muscle mass and muscle capillarization. These muscle-specific features of diabetes may, in turn, compromise insulin sensitivity and glucose control. Using a model of streptozotocin-induced diabetes, we show the vascular complications linked with disease and how chronic exposure to exercise and Prazosin (an alpha1-adrenergic antagonist) can reduce these complications and improve glycemic control.

The efficacy of prazosin for the treatment of posttraumatic stress disorder nightmares in U.S. military veterans.[Pubmed:27977074]

J Am Assoc Nurse Pract. 2017 Feb;29(2):65-69.

BACKGROUND AND PURPOSE: Nightmares associated with posttraumatic stress disorder (PTSD) are a hallmark symptom among U.S. military veterans who have seen combat. Management of combat-related nightmares can be difficult and current pharmacologic options are limited and tend to have adverse side effects. The aim of this review is to explore recent literature regarding the efficacy of Prazosin for the treatment of nightmare disorder in the veteran population. METHODS: Recent literature consisting of three systematic reviews was reviewed, as well as current clinical guidelines published by The Department of Veterans Affairs (VA) and The Department of Defense (DoD) and the American Academy of Sleep Medicine (AASM). CONCLUSIONS: Prazosin has been shown to be effective in the treatment of PTSD trauma-related nightmares. As a result of its low side effect profile and abilities to improve both sleep and reduce trauma nightmares, Prazosin has been recommended as an adjunct therapy. IMPLICATIONS FOR PRACTICE: Prazosin should be initiated as an adjunctive treatment to promote sleep in those suffering from PTSD nightmares. It should be initiated at 1 mg and then titrated upward until absence or desired reduction of nightmares is achieved, with a maximum dosage recommendation of 20 mg at bedtime and 5 mg midmorning.

Prazosin in Children and Adolescents With Posttraumatic Stress Disorder Who Have Nightmares: A Systematic Review.[Pubmed:27930498]

J Clin Psychopharmacol. 2017 Feb;37(1):84-88.

BACKGROUND: The aim of this systematic review was to identify published articles that evaluated the use of Prazosin for treating nightmares in children and adolescents who have posttraumatic stress disorder (PTSD). PROCEDURES: A literature search was conducted of PubMed, MEDLINE, EMBASE, Cochrane Collaboration, and PsycINFO databases for published articles in any language that evaluated the use of Prazosin for treating nightmares in the context of PTSD in children and adolescents using the following key words: PTSD, nightmares, Prazosin, children, adolescents, trauma, and sleep. RESULTS: A total of 9 published articles related to the use of Prazosin for treatment of nightmares in PTSD in children and adolescents were identified. Six of the 9 articles that met our inclusion criteria were case reports. All of these 6 case reports showed marked improvement in nightmares when Prazosin was used, although at a generally lower dose when compared with its use in adults, with dosing ranging from 1 to 4 mg/d. CONCLUSIONS: Prazosin has shown promising outcomes in treating nightmares associated with PTSD in children and adolescents, although this has not been well studied. Future placebo-controlled trials are needed to assess the efficacy and safety of Prazosin in treating PTSD-related nightmares in children and adolescents.

Injections of the of the alpha1-adrenoceptor antagonist prazosin into the median raphe nucleus increase food intake and Fos expression in orexin neurons of free-feeding rats.[Pubmed:28212941]

Behav Brain Res. 2017 May 1;324:87-95.

Previously, we showed that the blockade of alpha1-adrenoreceptors in the median raphe nucleus (MnR) increased food intake in free-feeding rats, indicating that adrenergic mechanisms in the MnR participate in the regulation of food intake. However, the impact of such a pharmacological manipulation on other neural circuits related to food intake remains unknown. In the current study, we sought to identify forebrain regions which are responsive to alpha1-adrenergic receptor blockade and presumably involved in the modulation of the feeding response. For this purpose, we examined the induction of c-Fos immunoreactivity in forebrain structures following injections of the alpha1-adrenoceptor antagonist Prazosin into the MnR of free-feeding rats. To determine the chemical identity of hypothalamic c-Fos-positive cells, we then conducted double-label immunohistochemistry for Fos/orexin (OX) or Fos/melanin-concentrating hormone (MCH). Finally, we combined anterograde tracing from the MnR with immunohistochemical detection of orexin. Prazosin injections into the MnR significantly increased food intake. The ingestive response was accompanied by an increase in Fos expression in the basolateral amygdala (BLA) and lateral hypothalamic area (LHA). In the LHA, Fos expression occurred in neurons expressing OX, but not MCH. Combined anterograde tracing experiments revealed that LHA OX neurons are prominently targeted by MnR axons. These findings suggest that intra-MnR injection of Prazosin, via activation of orexinergic neurons in the LHA and non-orexinergic neurons in the BLA, evoked a motivational response toward food intake.

Prazosin is an alpha-adrenergic blocker and is a sympatholytic drug used to treat high blood pressure and anxiety, PTSD, and panic disorder.

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