NaHS relaxes rat cerebral artery in vitro via inhibition of l-type voltage-sensitive Ca2+ channel

Tian, Xiaoyu; Wong, Wing Tak; Sayed, Nazish; Luo, Jialie; Tsang, Suk Ying; Bian, Zhao Xiang; Lu, Yujiao; Cheang, Wai San; Yao, Xiaoqiang; Chen, Zhen Yu; Huang, Yü

doi:10.1016/j.phrs.2011.11.006

Cited by 53 publications

(46 citation statements)

References 41 publications

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“…Recently, Liu et al have reported that H 2 S decreased the myogenic response of cerebral arterioles in vivo, and this effect was endotheliumdependent and was partially mediated by K (ATP) channels (14). A recent study showed that NaHS, a H 2 S donor, dilated rat cerebral arteries primarily through inhibiting Ca 2+ influx via Ca 2+ channels (20).…”

Section: A B Cmentioning

confidence: 99%

“…When H 2 S inhibitors and donor were administered to the SAH animals, only NaHS exerted significant vasodilatory effect on basilar artery LD, suggesting that H 2 S plays a distinct role in cerebrovascular pathophysiology. The mechanism by which H 2 S acts to inhibit vasospasm might relate to its ability to inhibit Ca 2+ influx via Ca 2+ channels in rat cerebral arteries (20). However, the underlying cellular mechanisms related to the vascular effect of H 2 S remain to be examined in detail.…”

Section: A B Cmentioning

confidence: 99%

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The effect of hydrogen sulphide on experimental cerebral vasospasm

Emmez¹,

Börcek²,

Gönül³

et al. 2015

Turkish Neurosurgery

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Section: A B Cmentioning

confidence: 99%

Section: A B Cmentioning

confidence: 99%

The effect of hydrogen sulphide on experimental cerebral vasospasm

Emmez¹,

Börcek²,

Gönül³

et al. 2015

Turkish Neurosurgery

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“…The vasorelaxing action of NaHS, administrated at concentrations ranging from 50 µM to 100 µM, has been observed in rat aorta and hepatic artery [96,97], as well as in resistance mesenteric arteries [21], gastric artery and gastric mucosal circulation [98], cerebral arterioles and artery [99,100], pulmonary artery [101], and coronary artery [102]. Since NaHS is five-to-nine fold more potent in relaxing mesenteric arteries than thoracic aorta and pulmonary artery (EC 50 25 µM vs. 125 µM and 233 µM, respectively), it has been proposed as a key regulator of peripheral resistance arteries and, therefore, of blood pressure [15].…”

Section: The Roles Of H 2 S and No In Vasodilationmentioning

confidence: 99%

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

Altaany¹,

Moccia²,

Munaron³

et al. 2014

CMC

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The endothelium is a cellular monolayer that lines the inner surface of blood vessels and plays a central role in the maintenance of cardiovascular homeostasis by controlling platelet aggregation, vascular tone, blood fluidity and fibrinolysis, adhesion and transmigration of inflammatory cells, and angiogenesis. Endothelial dysfunctions are associated with various cardiovascular diseases, including atherosclerosis, hypertension, myocardial infarction, and cardiovascular complications of diabetes. Numerous studies have established the antiinflammatory, anti-apoptotic, and anti-oxidant effects of hydrogen sulfide (H 2 S), the latest member to join the gasotransmitter family along with nitric oxide and carbon monoxide, on vascular endothelium. In addition, H 2 S may prime endothelial cells (ECs) toward angiogenesis and contribute to wound healing, aside to its well-known ability to relax vascular smooth muscle cells (VSMCs), thereby reducing blood pressure. Finally, H 2 S may inhibit VSMC proliferation and platelet aggregation. Consistently, a deficit in H 2 S homeostasis is involved in the pathogenesis of atherosclerosis and of hyperglycaemic endothelial injury. Therefore, the application of H 2 S-releasing drugs or using gene therapy to increase endogenous H 2 S level may help restore endothelial function and antagonize the progression of cardiovascular diseases. The present article reviews recent studies on the role of H 2 S in endothelial homeostasis, under both physiological and pathological conditions, and its putative therapeutic applications. Endothelial structure and functionThe endothelium lines the luminal surface of the entire vascular tree and the cardiac chambers, where it is termed endocardium. As a consequence, the endothelium presents a rather broad extension (300 to 1000 m 2 ) and weight (1.5 kg), achieving sizes comparable to other vital organs of the human body [1,2]. The endothelium can, therefore, be regarded as a real "organ spread across the organism" [3] and, as such, not only it is important for the regulation of local tissue functions, but also for maintaining the whole organism homeostasis [4]. Vascular endothelial cells (ECs) possess a polarized architecture: their luminal membrane is directly exposed to hematic constituents and circulating cells, while the basolateral surface is separated from surrounding tissues by a glycoprotein basement membrane -the sub-endothelial basement -which is formed by fibronectin, laminin, and collagen and is secreted by ECs themselves [2].Heterogeneity is, however, the hallmark of endothelium. ECs differ in morphology, function, and gene expression profile, so that even neighbouring cells from the same organ and blood vessel type exhibit distinct features [4]. For instance, vascular ECs may vary in size, shape, thickness and position of the nucleus. Albeit oriented along direction of blood flow, to attenuate the impact of shear stress forces on the vascular wall, microvascular ECs are rather thin (0.1 µm) and spindle-like, whilst their macrovascul...

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“…Біологічні ефекти H 2 S пов'язані з регуляцією серцево-судинної, імунної, ен-докринної, видільної, сенсорної та нервової систем [4][5][6][7][8]. Однак однією з найважливіших властивостей сірководню є його потужна судинорозширювальна дія [9,10].…”

Section: вступunclassified

“…Висока внутрішньоклітинна концент ра ція кальцію є необхідною умовою розвитку скорочення ГМК. Закриття цих каналів спричиняє зменшення концентрації вільно-го внутрішньоклітинного кальцію [9]. Тому інгібування потенціалзалежних каль ціє-вих каналів викликає зниження внутріш-ньоклітинної концентрації кальцію та роз-слаб лення судин.…”

Section: показникиunclassified

Тне Rоle of Hydrogen Sulfide in Regulation of Circulation Blood Liver

Yanchuk¹,

Slobodianyk²

2015

Fiziol Zh

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NaHS relaxes rat cerebral artery in vitro via inhibition of l-type voltage-sensitive Ca2+ channel

Cited by 53 publications

References 41 publications

The effect of hydrogen sulphide on experimental cerebral vasospasm

The effect of hydrogen sulphide on experimental cerebral vasospasm

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

Тне Rоle of Hydrogen Sulfide in Regulation of Circulation Blood Liver

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