Aspirin blocks nicotinic acid–induced flushing

Wilkin, Jonathan K.; Wilkin, O.; Kapp, Ronald; Donachie, Robert; Chernosky, Marvin E.; Buckner, Joyce

doi:10.1038/clpt.1982.63

Cited by 78 publications

(37 citation statements)

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“…However PGE 2 levels also increase in response to niacin (Eklund et al, 1979;Kobza Black et al, 1982). In man, the flush response to niacin can be completely abolished by COX inhibitors such as aspirin or indomethacin (Svedmyr et al, 1977;Wilkin et al, 1982). In mice, the flush response to niacin can be eliminated by knocking out genes for either the niacin receptor or COX-1, consistent with an exclusive and obligatory role for this pathway in niacin-evoked skin flushing (Benyó et al 2005).…”

Section: Mediation Of Niacin Flush By Aa Metabolitesmentioning

confidence: 62%

Phospholipid, arachidonate and eicosanoid signaling in schizophrenia

Messamore

Yao

2015

OCL

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-This paper reviews the potential role of arachidonic acid in the pathophysiology of schizophrenia. We discuss how abnormal levels of arachidonic acid may arise, and how dysregulation of signaling molecules derived from it have the potential to disrupt not only dopamine signaling, but numerous other physiological processes associated with the illness. Pharmacological doses of niacin stimulate the release of arachidonic acid; and arachidonic acid-derived molecules in turn dilate blood vessels in the skin. A blunted skin flush response to niacin is reliably observed among patients with schizophrenia. The niacin response abnormality may thus serve as a biomarker to identify a physiological subtype of schizophrenia associated with defective arachidonic acid-derived signaling.Keywords: Phospholipids / arachidonic acid / eicosanoids / niacin-induced flushing, endophenotype marker / schizophrenia Résumé -Signalisation des phospholipides, de l'arachidonate et de l'écosanoïde dans la schizophrénie. Cet article examine le rôle potentiel de l'acide arachidonique dans la physiopathologie de la schizophrénie. Il est discuté comment des niveaux anormaux d'acide arachidonique peuvent survenir, et comment la dérégulation des molécules de signalisation qui en découle est capable de perturber non seulement la signalisation de la dopamine, mais aussi de nombreux autres processus physiologiques associés avec cette maladie. Des doses pharmacologiques de niacine stimulent la libération d'acide arachidonique ; des molécules dérivées de l'acide arachidonique dilatent à leur tour les vaisseaux sanguins dans la peau. Une brusque rougeur de la peau en réponse à la niacine est observée de manière constante parmi les patients atteints de schizophrénie. La réponse anormale à la niacine peut donc servir de biomarqueur afin d'identifier un sous-type physiologique de la schizophrénie, associé à un système défectueux de signalisation des dérivés de l'acide arachidonique.

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Section: Mediation Of Niacin Flush By Aa Metabolitesmentioning

confidence: 62%

Phospholipid, arachidonate and eicosanoid signaling in schizophrenia

Messamore

Yao

2015

OCL

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“…However, it has now been well established that both methyl nicotinate and nicotinic acid-induced flushing response is the result of increased prostaglandin synthesis in skin cells, suggested to be macrophages or adipocytes, which then act upon capillary epithelial cells to cause vasodilation (Wilkin et al, 1982(Wilkin et al, , 1985Morrow et al, 1989;Turenne et al, 2001). Interestingly, healthy subjects develop tolerance to the nicotinic acid-induced flushing response (Stern et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Methyl Nicotinate-Induced Vasodilation in Generalized Social Phobia

Katzman

Cornacchi

Coonerty-Femiano

et al. 2003

Neuropsychopharmacol

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Elevated vasodilatory response (blushing) to social situations is characteristic of social phobia (SP). A relatively unexplored basis for this phenomenon is alteration in underlying vasodilatory mechanisms. To investigate this possibility, we evaluated the vasodilatory response induced by methyl nicotinate (niacin ester derivative) in 31 generalized SP patients and 41 matched healthy volunteers (HV). A patch impregnated with 0, 0.1, 0.5, 1, and 10 mM methyl nicotinate was applied to the forearm or face of subjects for 1 min, followed by 20-min laser Doppler spectroscopy blood flow monitoring. Blood flow stimulation with 1 and 10 mM methyl nicotinate was significantly reduced in SP patients by 35 and 17%, respectively. Induced blood flow was negatively correlated with patients' Leibowitz Social Phobia Scale (LSAS) at 1 and 10 mM doses. Furthermore, the maximal rate of change of vasodilatory reaction was correlated with symptom scores at 1 and 10 mM doses. Induced increases in the arm and face blood flow measurements correlated, supporting the external validity of the former location. Generalized SP patients vasodilate less to topical methyl nicotinate challenges, with effect amplification in severely ill patients. Although the mechanism for this is unclear, we propose desensitization of the prostaglandin-mediated vasodilating system as an explanation.

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“…Obwohl in vielen Fällen eine Toleranzentwicklung gegenüber dieser prostaglandinvermittelten Reaktion erwartet werden kann [49], sind verschiedene Maßnahmen vorgeschlagen worden, diesen Effekt abzumildern und damit die Compliance der Patienten zu verbessern. Zum einen kann die Schwere der FlushSymptomatik durch die Gabe von 325 mg Acetylsalicylsäure 1 h vor Niacineinnahme gesenkt werden [50]. Zum anderen besteht die Möglichkeit einer abendlichen Gabe von Niacin, wodurch die Flush-Symptomatik vom Patienten während des Schlafens nicht wahrgenommen wird [29].…”

Section: Unerwünschte Wirkungen Unter Nikotinsäureunclassified