Comparison of H2O2-induced vasoconstriction in the abdominal aorta and mesenteric artery of the mouse

被引:12
作者
Ardanaz, Noelia [1 ]
Beierwaltes, William H. [1 ]
Pagano, Patrick J. [1 ]
机构
[1] Henry Ford Hlth Syst, Hypertens & Vasc Res Div, Detroit, MI 48202 USA
关键词
hydrogen peroxide; vasoconstriction; abdominal aorta; superior mesenteric artery; depolarization; tyrosine kinase; mitogen-activated protein kinases; rho-kinase;
D O I
10.1016/j.vph.2007.08.007
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Hydrogen peroxide (H2O2) is generally perceived as an arterial vasodilator. Due to the emerging importance of H2O2 as a possible vasoconstrictor, we examined whether H2O2 constricts both the abdominal aorta and superior mesenteric artery and postulated that H2O2 is a ubiquitous constrictor of quiescent mouse arteries. Moreover, we postulated that KCl depolarization discloses and/or exaggerates H2O2-induced constriction. Under quiescent conditions, H2O2 constricted the mouse abdominal aorta but not the mesenteric artery. Vessel depolarization (a) exaggerated this constrictor response in the aorta, and (b) unmasked a contractile response in the mesenteric artery. Our final hypothesis tested whether tyrosine kinases, mitogen-actvated protein kinases (MAPKs), and/or Rho-kinase are uniformly involved in H2O2-induced vasoconstriction. We observed a marked difference in the ability of tyrosine kinase inhibitor to block H2O2-induced vasoconstriction. p38 and ERK 1/2MAPK inhibitors reduced the maximal response to H2O2, whereas JNK inhibitor had no effect. Finally, Rho-kinase inhibitor decreased the H2O2 response in the mesenteric artery but not in the aorta. These data demonstrate a variable yet tightly regulated H2O2 vasoconstrictor effect. Furthermore, we found that p38, ERK 1/2 and Rho-kinase play a role in H2O2 constriction, which may be critical pathways involved in H2O2-induced constriction across vascular beds. © 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:288 / 294
页数:7
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