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      Neuropsychiatric Disease and Treatment (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on all aspects of neuropsychiatric and neurological disorders. Sign up for email alerts here.

      63,741 Monthly downloads/views I 2.989 Impact Factor I 4.5 CiteScore I 1.09 Source Normalized Impact per Paper (SNIP) I 0.744 Scimago Journal & Country Rank (SJR)

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      Worsened hypertension control induced by aripiprazole

      case-report

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          Abstract

          Aripiprazole is widely used in the treatment of schizophrenia and bipolar disorders. Although antipsychotics generally have hypotensive effects, two cases were identified that demonstrated hypertension during the switch from other antipsychotics to aripiprazole. The hypertensive state of these patients recovered after switching back to other antipsychotics, and these cases suggest that aripiprazole may lead to hypertension.

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          The antipsychotic aripiprazole is a potent, partial agonist at the human 5-HT1A receptor.

          Martha Jordan, Katsura Tottori, C Anthony Altar … (2002)
          Aripiprazole, 7-[4-[4-(2,3-dichlorophenyl)-1-piperazinyl]butyloxy]-3,4-dihydro-2(1H)-quinolinone, a novel antipsychotic with partial agonist activity at dopamine D2 receptors, bound with high affinity to recombinant human 5-HT(1A) receptors (h5-HT(1A)) in Chinese hamster ovary cell membranes and displayed potent, partial agonism at 5-HT(1A) receptors in a guanosine-5'-O-(3-[(35)S]thio)-triphosphate ([(35)S]GTP gamma S)-binding assay that was blocked completely by a selective 5-HT(1A) receptor antagonist. An interaction with 5-HT(1A) receptors may contribute to the overall efficacy of aripiprazole against symptoms of schizophrenia, including anxiety, depression, cognitive and negative symptoms, and to its favorable side-effect profile. Combined with previous studies demonstrating the potent partial agonism of aripiprazole at dopamine D2 receptors, this study suggests aripiprazole is the first dopamine-serotonin system stabilizer.
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            Inhibitory effects of aripiprazole on interferon-gamma-induced microglial activation via intracellular Ca2+ regulation in vitro.

            O Suzuki, Yoshihiro Seki, Hideki Horikawa … (2008)
            The activation of the inflammatory/immunological response system is suggested to be related to the pathophysiology of schizophrenia. Aripiprazole is a novel atypical antipsychotic, which is a high-affinity dopamine D(2) receptor partial agonist. Atypical antipsychotics, all of which have dopamine D(2) receptor antagonism, have recently reported to have significantly inhibitory effects on interferon (IFN)-gamma-induced microglial activation in vitro. In the present study, we investigated whether or not aripiprazole also has anti-inflammatory effect on IFN-gamma-induced microglial activation. Not quinpirole, dopamine D(2) full agonist, but aripiprazole significantly inhibited the generation of nitric oxide (NO) and tumor necrosis factor (TNF)-alpha from IFN-gamma-activated microglia and suppressed the IFN-gamma-induced elevation of intracellular Ca(2+) concentrations ([Ca(2+)](i)) in murine microglial cells. Increased [Ca(2+)](i) has been reported to be required, but by itself not sufficient, for the release of NO and certain cytokines. As a result, we can speculate that aripiprazole may inhibit IFN-gamma-induced microglial activation through the suppression of IFN-gamma-induced elevation of [Ca(2+)](i) in microglia. Our results demonstrated that not only antipsychotics which have dopamine D(2) receptor antagonism but also aripiprazole have anti-inflammatory effects via the inhibition of microglial activation. Antipsychotics may therefore have a potentially useful therapeutic effect on patients with schizophrenia by reducing the microglial inflammatory reactions.
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              Mechanism of action of aripiprazole predicts clinical efficacy and a favourable side-effect profile.

              Kevin D Burris, Y Uwahodo, H Kitagawa … (2004)
              The antipsychotic efficacy of aripiprazole is not generally associated with extrapyramidal symptoms, cardiovascular effects, sedation or elevations in serum prolactin that characterize typical or atypical antipsychotics. The aim of this study was to clarify the mechanism of action of aripiprazole that underlies its favourable clinical profiles. The preclinical efficacy and side-effect profiles of aripiprazole were evaluated using several pharmaco-behavioural test systems in mice and rats, both in vivo and ex vivo, and compared with those of other conventional and atypical antipsychotics. Each of the antipsychotics induced catalepsy and inhibited apomorphine-induced stereotypy. The catalepsy liability ratios for these drugs were 6.5 for aripiprazole, 4.7 for both olanzapine and risperidone. The ptosis liability ratios for aripiprazole, olanzapine and risperidone were 14, 7.2 and 3.3, respectively. Aripiprazole slightly increased DOPA accumulation in the forebrain of reserpinised mice, reduced 5-HTP accumulation at the highest dose and exhibited a weaker inhibition of 5-methoxy-N,N-dimethyl-tryptamine-induced head twitches. Aripiprazole did not inhibit physostigmine- or norepinephrine-induced lethality in rats. In conclusion, aripiprazole shows a favourable preclinical efficacy and side-effect profile compared to a typical antipsychotics. This profile may result from its high affinity partial agonist activity at D2 and 5-HT1A receptors and its antagonism of 5-HT2A receptors.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neuropsychiatr Dis Treat
                Journal ID (iso-abbrev): Neuropsychiatr Dis Treat
                Journal ID (publisher-id): Neuropsychiatric Disease and Treatment
                Title: Neuropsychiatric Disease and Treatment
                Publisher: Dove Medical Press
                ISSN (Print): 1176-6328
                ISSN (Electronic): 1178-2021
                Publication date Collection: 2013
                Publication date (Print): 2013
                Publication date (Electronic): 15 April 2013
                Volume: 9
                Pages: 505-507
                Affiliations
                Department of Neuropsychiatry, Graduate School of Medicine, Hirosaki University, Hirosaki, Japan
                Author notes
                Correspondence: Norio Yasui-Furukori, Department of Neuropsychiatry, Graduate School of Medicine, Hirosaki University, Hirosaki 036-8562, Japan, Tel +81 172 395 066, Fax +81 172 395 067, Email yasufuru@ 123456cc.hirosaki-u.ac.jp
                Article
                Publisher ID: ndt-9-505
                DOI: 10.2147/NDT.S43950
                PMC ID: 3666545
                PubMed ID: 23723701
                SO-VID: 22e5c2cc-9cd9-4515-a6b6-fe95454030fa
                Copyright © © 2013 Yasui-Furukori and Fujii, publisher and licensee Dove Medical Press Ltd.
                License:

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                History
                Categories
                Subject: Case Report

                ScienceOpen disciplines: Neurology
                Keywords: hypertension,aripiprazole,dopamine antagonist,5-ht1a
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: hypertension, aripiprazole, dopamine antagonist, 5-ht1a

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