The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

Sun, Yan; Tang, Chaoshu; Jin, Hongfang; Du, Junbao

doi:10.1038/aps.2011.9

Cited by 24 publications

(26 citation statements)

References 40 publications

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“…CBS proteins were observed in rat pulmonary artery rings (Sun et al 2011) and bovine pulmonary artery endothelial cells (Olson et al 2010). In rat hepatic artery and portal vein, both CSE and CBS proteins were localized, but interestingly the terminal branches of the hepatic afferent vessels only expressed CSE (Siebert et al 2008).…”

Section: Endogenous Production Of H S In Blood Vesselsmentioning

confidence: 97%

“…The opening of K ATP channels hyperpolarizes cell membrane and inactivates voltage-dependent L-type Ca 2+ channels, leading to cell relaxation and blood vessel dilation by reducing intracellular free Ca 2+ concentration (Wang 2012a, b). It has been previously shown that H 2 S at physiologically relevant concentrations induced the relaxation of rat aortic tissue and transient reduction of blood pressure, and these vascular effects of H 2 S were mediated by a direct stimulation of K ATP channels and subsequent hyperpolarization of aortic SMCs (Zhao et al 2001;Cheng et al 2004;Wang 2014;Sun et al 2011;Siebert et al 2008). Using the whole-cell and single-channel patch-clamp technique, Tang et al demonstrated that H 2 S activates K ATP channels and hyperpolarized cell membrane in rat mesenteric artery SMCs (Tang et al 2005.…”

Section: H 2 S and Smc Relaxation And Contractionmentioning

confidence: 99%

“…Following studies have demonstrated endothelial expression of CSE in mice, rats, and humans (Altaany et al 2013;Papapetropoulosa et al 2009). To date, CSE proteins and/or mRNA have been detected in newborn pig cerebral microvessels (Leffler et al 2011), mouse renal artery SMCs (Sen et al 2012b), rat pulmonary artery SMCs and ECs (Sun et al 2011;Chen et al 2009), mouse pulmonary artery SMCs and ECs , human pulmonary artery SMCs (Kiss et al 2008), bovine pulmonary artery SMCs and sea lion resistance pulmonary arteries (Olson et al 2010), rat hepatic artery and portal vein (Siebert et al 2008), and human internal mammary artery (Webb et al 2008).…”

Section: Endogenous Production Of H S In Blood Vesselsmentioning

confidence: 99%

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H2S and Blood Vessels: An Overview

Yang

Wang

2015

Handbook of Experimental Pharmacology

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The physiological and biomedical importance of hydrogen sulfide (H2S) has been fully recognized in the cardiovascular system as well as in the rest of the body. In blood vessels, cystathionine γ-lyase (CSE) is a major H2S-producing enzyme expressed in both smooth muscle and endothelium as well as periadventitial adipose tissues. Regulation of H2S production from CSE is controlled by a complex integration of transcriptional, posttranscriptional, and posttranslational mechanisms in blood vessels. In smooth muscle cells, H2S regulates cell apoptosis, phenotypic switch, relaxation and contraction, and calcification. In endothelial cells, H2S controls cell proliferation, cellular senescence, oxidative stress, inflammation, etc. H2S interacts with nitric oxide and acts as an endothelium-derived relaxing factor and an endothelium-derived hyperpolarizing factor. H2S generated from periadventitial adipose tissues acts as an adipocyte-derived relaxing factor and modulates the vascular tone. Extensive evidence has demonstrated the beneficial roles of the CSE/H2S system in various blood vessel diseases, such as hypertension, atherosclerosis, and aortic aneurysm. The important roles signaling in the cardiovascular system merit further intensive and extensive investigation. H2S-releasing agents and CSE activators will find their great applications in the prevention and treatment of blood vessel-related disorders.

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Section: Endogenous Production Of H S In Blood Vesselsmentioning

confidence: 97%

Section: H 2 S and Smc Relaxation And Contractionmentioning

confidence: 99%

Section: Endogenous Production Of H S In Blood Vesselsmentioning

confidence: 99%

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H2S and Blood Vessels: An Overview

Yang

Wang

2015

Handbook of Experimental Pharmacology

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“…Although they are still unclear, the mechanisms by which H 2 S influences the heart and coronary circulation probably include activation of K ATP channels in both cardiomyocytes (47) and coronary smooth muscles (37). Despite the insufficient knowledge of the role of H 2 S in the heart functioning, the coronary circulation and the discrepancy between the existing data, this gasotransmitter can obviously be synthesized in the heart, and together with…”

Section: Discussionmentioning

confidence: 99%

The role of hydrogen sulfide in homocysteine-induced cardiodynamic effects and oxidative stress markers in the isolated rat heart

et al. 2016

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This study aimed to assess the role of H 2 S in homocysteine-induced cardiodynamic effects in the isolated rat heart. The hearts were retrogradely perfused according to the Langendorff technique. The maximum and minimum rates of pressure in the left ventricle (dp/dt max, dp/dt min), systolic and diastolic left ventricular pressures (SLVP, DLVP), heart rate (HR), and coronary flow (CF) were measured. A spectrophotometrical method was used to measure the following oxidative stress markers: index of lipid peroxidation (thiobarbituric acid reactive substances, TBARS), nitrite level (NO 2 − ), superoxide anion radicals (O 2• − ), and hydrogen peroxide (H 2 O 2 ) concentrations. The administration of 10 μmol/l DL-homocysteine (DL-Hcy) alone decreased dp/dt max, SLVP, and CF but did not change any oxidative stress parameters. The administration of 10 μmol/l DL-propargylglycine (DL-PAG) decreased all cardiodynamic parameters and increased the concentration of O 2• − .The co-administration of DL-Hcy and DL-PAG induced a significant decrease in all estimated cardiodynamic parameters and decreased the concentration of NO 2 − and O 2 • − but increased the levels of TBARS and H 2 O 2 .Homocysteine shows a lower pro-oxidative effect in the presence of hydrogen sulfide (H 2 S), which indicates a potential anti-oxidative capacity of H 2 S.

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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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The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

Cited by 24 publications

References 40 publications

H2S and Blood Vessels: An Overview

H2S and Blood Vessels: An Overview

The role of hydrogen sulfide in homocysteine-induced cardiodynamic effects and oxidative stress markers in the isolated rat heart

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

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