Contributory role of endothelium and voltage-gated potassium channels in apocynin-induced vasorelaxations

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review

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Author(s)

  • Wei-Qing Han
  • Wing Tak Wong
  • Xiao Yu Tian
  • Ling-Yun Wu
  • Ding-Liang Zhu
  • Ping-Jin Gao

Detail(s)

Original languageEnglish
Pages (from-to)2102-2110
Journal / PublicationJournal of Hypertension
Volume28
Issue number10
Publication statusPublished - Oct 2010
Externally publishedYes

Abstract

Objective: Although apocynin, the nicotinamide adenine dinucleotide phosphate oxidase inhibitor improves vascular function in hypertension, its specificity has been questioned. The present study examined whether apocynin-induced vasorelaxations involve endothelium and/or K channels in vascular cells. Methods: Aortas from Sprague-Dawley rats were suspended in organ baths for functional studies. Changes in intracellular calcium ([Ca <sup>2+</sup>]<sub>i</sub>) and nitric oxide ([NO]<sub>i</sub>) in rat endothelial cells were detected by fluorescence imaging. Whole-cell voltage-gated K<sup>+</sup>(Kv) currents were recorded in vascular smooth muscle cells. Results: Apocynin-induced aortic relaxations were attenuated by the absence of endothelium, endothelial nitric oxide synthase inhibitor N <sup>G</sup>-nitro-L-arginine methyl ester, or nitric oxide-dependent soluble guanylate cyclase inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one. 4-Aminopyridine (4-AP, voltage-gated potassium channels blocker) attenuated apocynin-induced relaxations, its combined treatment with 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ) did not cause further inhibition. Apocynin increased [Ca<sup>2+</sup>]<sub>i</sub> and [NO]<sub>i</sub> in endothelial cells, which were abolished by 4-AP, indicating the involvement of voltage-gated potassium channels in endothelial cells. In addition, apocynin-stimulated increase in endothelial nitric oxide synthase phosphorylation at Ser <sup>177</sup> depended on the presence of extracellular Ca<sup>2+</sup>. Notably, 4-AP also reduced apocynin-induced relaxations in the absence of endothelium and apocynin increased 4-AP-sensitive voltage-gated potassium channel currents in vascular smooth muscle cells. Conclusion: This study provides novel data showing that apocynin-induced relaxations of rat aortas are mediated by 4-AP-sensitive stimulation of [Ca<sup>2+</sup>]<sub>i</sub> and [NO]<sub>i</sub> increases in endothelium and by activation of voltage-gated potassium channels in vascular smooth muscle cells. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Research Area(s)

  • apocynin, endothelium, nitric oxide, potassium channel

Bibliographic Note

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Citation Format(s)

Contributory role of endothelium and voltage-gated potassium channels in apocynin-induced vasorelaxations. / Han, Wei-Qing; Wong, Wing Tak; Tian, Xiao Yu; Huang, Yu; Wu, Ling-Yun; Zhu, Ding-Liang; Gao, Ping-Jin.

In: Journal of Hypertension, Vol. 28, No. 10, 10.2010, p. 2102-2110.

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review