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- Title
Mitochondrial Fission Inhibitors Suppress Endothelin-1-Induced Artery Constriction.
- Authors
Chen, Chang; Gao, Jin-Lai; Liu, Ming-Yu; Li, Shan-Liang; Xuan, Xiu-Chen; Zhang, Xin-Zi; Zhang, Xi-Yue; Wei, Yuan-Yuan; Zhen, Chang-Lin; Jin, Jing; Shen, Xin; Dong, De-Li
- Abstract
Background/Aims: Endothelin-1 is implicated in the pathogenesis of hypertension, but the underlying mechanisms remained elusive. Our previous study found that inhibition of mitochondrial fission of smooth muscle cells suppressed phenylephrine- and high K+-induced artery constriction. Here, we studied the effects of mitochondrial fission inhibitors on endothelin-1-induced vasoconstriction. Methods: The tension of rat mesenteric arteries and thoracic aorta was measured by using a multi-wire myograph system. Mitochondrial morphology of aortic smooth muscle cells was observed by using transmission electron microscopy. Results: Dynamin-related protein-1 selective inhibitor mdivi-1 relaxed endothelin-1-induced constriction, and mdivi-1 pre-treatment prevented endothelin-1-induced constriction of rat mesenteric arteries with intact and denuded endothelium. Mdivi-1 had a similar inhibitory effect on rat thoracic aorta. Another mitochondrial fission inhibitor dynasore showed similar effects as mdivi-1 in rat mesenteric arteries. Mdivi-1 inhibited endothelin-1-induced increase of mitochondrial fission in smooth muscle cells of rat aorta. Rho-associated protein kinase inhibitor Y-27632 which relaxed endothelin-1-induced vasoconstriction inhibited endothelin-1-induced mitochondrial fission in smooth muscle cells of rat aorta. Conclusion: Endothelin-1 increases mitochondrial fission in vascular smooth muscle cells, and mitochondrial fission inhibitors suppress endothelin-1-induced vasoconstriction.
- Subjects
PREPROENDOTHELIN; VASCULAR smooth muscle; HYPERTENSION genetics; PROTEIN kinase inhibitors; MITOCHONDRIAL pathology
- Publication
Cellular Physiology & Biochemistry (Karger AG), 2017, Vol 42, Issue 5, p1802
- ISSN
1015-8987
- Publication type
Article
- DOI
10.1159/000479536