Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/47873
Title: Hydroxychloroquine induces endothelium-dependent and endothelium-independent relaxation of rat aorta
Authors: Arslan, Seyfullah Oktay
Doğan, Muhammet Fatih
Çam, Saliha Ayşenur
Omar, Ibraheem Akram
Uysal, Fatma
Parlar, Ali
Andaç, A.Cenk
Yıldız, Oğuzhan
Keywords: calcium channels
Hydroxychloroquine
nitric oxide
vasodilation
acetylcholine
alpha 1 adrenergic receptor stimulating agent
barium chloride
calcium
calcium channel
calcium channel blocking agent
calcium chloride
glibenclamide
hydroxychloroquine
hydroxychloroquine sulfate
indometacin
ketamine
n(g) nitroarginine methyl ester
nilvadipine
nitric oxide synthase
nitric oxide synthase inhibitor
phenylephrine
potassium channel
potassium channel blocking agent
prostaglandin synthase
tetrylammonium
xylazine
calcium chloride
indometacin
n(g) nitroarginine methyl ester
vasodilator agent
animal experiment
animal model
animal tissue
antimalarial activity
aorta
Article
autoimmune disease
connective tissue
controlled study
data analysis software
endothelium
female
nonhuman
rat
rheumatoid arthritis
vascular ring
vasodilatation
animal
aorta
dose response
endothelium
vascular endothelium
Animals
Aorta
Calcium Chloride
Dose-Response Relationship, Drug
Endothelium
Endothelium, Vascular
Hydroxychloroquine
Indomethacin
NG-Nitroarginine Methyl Ester
Rats
Vasodilator Agents
Publisher: Turkiye Klinikleri
Abstract: Background/aim: Hydroxychloroquine (HCQ) is an antimalarial that is widely used in the management of rheumatoid arthritis and other autoimmune diseases. In this study, we aimed to examine the vascular effects of HCQ on rat aorta (RA). Materials and methods: The RA rings were suspended in isolated organ baths and tension was recorded isometrically. HCQ-induced relaxations were tested in the presence of the nitric oxide synthase inhibitor, nitro-L-arginine methyl ester (L-NAME, 100 mM); the cyclooxygenase enzyme inhibitor, indomethacin (10 mM); the calcium (Ca2+) ion channel blocker, nilvadipine (10 ?M); and the K+ ion channel inhibitors, tetraethylammonium (1 mM), glibenclamide (10 mM), 4-aminopyridine (1 mM), and barium chloride (30 mM). The effect of HCQ on Ca2+ channels was examined using Ca2+-free Krebs solution, and adding calcium chloride (CaCl2, 10-5– 10-2 M) cumulatively to baths incubated with HCQ. Results: Removing the endothelium resulted in less relaxation of RA rings compared to endothelium-intact rings (p < 0.05). The effect of endothelium was supported by using L-NAME where HCQ produced-vasorelaxation was decreased (p < 0.05). The contraction of vascular rings was inhibited to a significant degree following the addition of CaCl2, PE, or KCl on HCQ-incubated RA rings (p < 0.05). The incubation of the RA rings with the Ca2+ channel blocker, the K+ channel blockers, and the COX inhibitor, indomethacin did not significantly affect vascular relaxation induced by HCQ. Conclusion: HCQ produced relaxation of RA rings. The relaxation mechanism differs according to the concentration of HCQ. At concentrations of 10-6 and 10-5 M, the relaxation is endothelium-dependent and mediated by NO. We strongly suggest that Ca2+ channel inhibition is involved at concentrations of 10-5 and 10-4 M, as well as NO. © TÜBİTAK.
URI: https://doi.org/10.55730/1300-0144.5382
https://search.trdizin.gov.tr/yayin/detay/536657
https://hdl.handle.net/11499/47873
ISSN: 1300-0144
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
TR Dizin İndeksli Yayınlar Koleksiyonu / TR Dizin Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

Show full item record



CORE Recommender

SCOPUSTM   
Citations

2
checked on Oct 13, 2024

WEB OF SCIENCETM
Citations

2
checked on Oct 31, 2024

Page view(s)

46
checked on Aug 24, 2024

Google ScholarTM

Check




Altmetric


Items in GCRIS Repository are protected by copyright, with all rights reserved, unless otherwise indicated.