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 Nov 21, 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.