On the inhibitory effect of chloroquine on blood platelet aggregation

Jančinová, Viera; Nosáľ, R; Petríková, M.

doi:10.1016/0049-3848(94)90270-4

Cited by 77 publications

(41 citation statements)

References 21 publications

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“…The efficacy of chloroquine in the therapy of porphyria cutanea tarda (69) could be mediated by NO, which has been reported to inhibit heme synthesis (2). On the other hand, an increased NO production may account for some side effects of chloroquine, mainly observed after treatment with high doses of drug or during parenteral administration: inhibition of platelet aggregation (70), transient hypotension (71), reduced forearm vascular resistance (72), in vivo vasodilation (73), mutagenic effects (74), and neuropathies (75). If so, NOS inhibitors could be associated to high dosage chloroquine treatment to prevent the onset of several toxic effects of the drug.…”

Section: Discussionmentioning

confidence: 99%

Chloroquine stimulates nitric oxide synthesis in murine, porcine, and human endothelial cells.

Ghigo

Aldieri²,

Todde³

et al. 1998

J. Clin. Invest.

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Nitric oxide (NO) is a free radical involved in the regulation of many cell functions and in the expression of several diseases. We have found that the antimalarial and antiinflammatory drug, chloroquine, is able to stimulate NO synthase (NOS) activity in murine, porcine, and human endothelial cells in vitro: the increase of enzyme activity is dependent on a de novo synthesis of some regulatory protein, as it is inhibited by cycloheximide but is not accompanied by an increased expression of inducible or constitutive NOS isoforms. Increased NO synthesis is, at least partly, responsible for chloroquine-induced inhibition of cell proliferation: indeed, NOS inhibitors revert the drug-evoked blockage of mitogenesis and ornithine decarboxylase activity in murine and porcine endothelial cells. The NOS-activating effect of chloroquine is dependent on its weak base properties, as it is exerted also by ammonium chloride, another lysosomotropic agent.

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Section: Discussionmentioning

confidence: 99%

Chloroquine stimulates nitric oxide synthesis in murine, porcine, and human endothelial cells.

Ghigo

Aldieri²,

Todde³

et al. 1998

J. Clin. Invest.

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“…HCQ can also reduce ADP-induced and/or ristocetin platelet aggregation [23,24], as well as arachidonic acid release by activated platelets [26].…”

Section: A-hcq Inhibits Platelet Aggregationmentioning

confidence: 99%

“…Therefore, HCQ could exert some antithrombotic effects through several mechanisms involving platelet adhesion, intravascular aggregation of red blood cells (RBCs), interactions between platelets and coagulation factors and binding of antiphospholipid (aPL) antibodies phospholipid surfaces [22][23][24][25][26][27][28][29][30][31].…”

Section: Contents Lists Available At Sciencedirectmentioning

confidence: 99%

Hydroxychloroquine as an anti-thrombotic in antiphospholipid syndrome

Bélizna

2015

Autoimmunity Reviews

108

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“…In addition to its anti-inflammatory effects, there are immunomodulatory effects of HCQ that include increasing the pH of intracellular vacuoles and interfering with antigen processing and inhibiting T-cell-receptor-induced and B-cellreceptor-induced calcium signaling [178,179]. HCQ also has antithrombotic effects by inhibiting platelet aggregation and arachidonic acid release from stimulated platelets [180].…”

Section: B Hydroxychloroquinementioning

confidence: 99%