Effects of H2S on Myogenic Responses in Rat Cerebral Arterioles

被引:19
|
作者
Liu, Lei [1 ]
Liu, Hong [2 ]
Sun, Dong [3 ,4 ]
Qiao, Weili [1 ]
Qi, Youjian [1 ]
Sun, Hong [1 ]
Yan, Changdong [1 ,3 ]
机构
[1] Xuzhou Med Coll, Dept Physiol, Xuzhou 221002, Jiangsu, Peoples R China
[2] Xuzhou Med Coll, Dept Pathol, Xuzhou 221002, Jiangsu, Peoples R China
[3] Xuzhou Med Coll, Jiangsu Prov Key Lab Anesthesiol, Xuzhou 221002, Jiangsu, Peoples R China
[4] New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA
关键词
Cerebral arterioles; Hydrogen sulfide; Myogenic reactivity; ENDOGENOUS HYDROGEN-SULFIDE; NITRIC-OXIDE; ENDOTHELIAL DYSFUNCTION; MESENTERIC ARTERIOLES; CARBON-MONOXIDE; VASCULAR-TONE; CYCLIC-GMP; ARTERY; HYPERTENSION; PREGNANCY;
D O I
10.1253/circj.CJ-11-0890
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: The potential biological significance of hydrogen sulfide (H2S) has attracted growing interests in recent years, but its role in the myogenic response of rat cerebral arterioles has not been explored. Methods and Results: Rats were injected with NaHS (an H2S donor, 2-200 mu mol.kg(-1).day(-1), i.p.) or saline for 3 weeks. MBP was measured with a tail-cuff method. C erebral arterioles were isolated and cannulated in an organ bath system, and vessel diameters were measured with an image-shearing device. Changes in diameter in response to stepwise increases in intravascular pressure (20-120 mmHg) were investigated under no-flow conditions. After the treatments, plasma H2S increased and MBP decreased significantly. NaHS reduced the myogenic response in a dose-dependent manner. This effect was markedly attenuated by glibenclamide, a K-ATP channel blocker. Blockade of nitric oxide (NO) production with NG-nitro-L-arginine methyl ester (L-NAME, a NO synthase inhibitor) enhanced, whereas removal of the endothelium abolished the inhibitory role of NaHS on the myogenic response. Conclusions: For the first time it has been demonstrated that H2S decreases the myogenic response of cerebral arterioles in vivo, and this effect is endothelium-dependent and partially mediated by K-ATP channels. (Circ J 2012; 76: 1012 1019)
引用
收藏
页码:1012 / 1019
页数:8
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