| 1. |
- Li, Jie, et al.
(författare)
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Heat stress alters G-protein coupled receptor-mediated function and endothelium-dependent relaxation in rat mesenteric artery
- 2008
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Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 1879-0712 .- 0014-2999. ; 588:2-3, s. 280-285
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Tidskriftsartikel (refereegranskat)abstract
- Heat stress has been demonstrated to have strong cardiovascular effects. However, the underlying mechanism-mediated cardiovascular effects are still not fully understood. The present study was designed to examine if heat stress alters vascular G-protein coupled receptor-mediated vasomotion and endothelium function in rat mesenteric artery. Rats were divided into two groups, heat stress rats and control. The G-protein coupled receptors of endothelin type B (ETB) receptor-, endothelin type A (ETA) receptor-, 5-hydroxytryptamine (5-HT) receptor-, calcitonin gene-related peptide (CGRP) receptor-, alpha-adrenoceptor-mediated vosoactivity and endothelium-dependent relaxation on rat mesenteric artery ring segments were monitored by a myograph system. The plasma level of CGRP was determined by radioimmunological assay. Compared with control arterial segments, the contractile response curves of sarafotoxin 6c, a selective ETB receptor agonist and 5-HT in the arterial segments from heat stress rats were shifted towards left. An increased maximum contraction (E-max) induced by sarafotoxin 6c, but not 5-HT, was seen in the arterial segments from heat stress rats. CGRP-incluced relaxation in endothelium-denuded arterial segments from heat stress rats was enhanced. The relaxation in endothelium-intact arterial segments induced by acetylcholine was significantly decreased in heat stress rats. In addition, the plasma concentration of CGRP was increased in heat stress rats. The endothelium-dependent relaxation was characterized and shown there was a decrease in nitric oxide and endothelium-derived hyperpolarising factor-mediated relaxation in the arterial segments from heat stress rats. In conclusion, heat stress induces an enhanced vascular endothelin ETB-, 5-HT-receptors-mediated contraction, an enhanced CGRP-receptor-induced relaxation and damage to endothelium-dependent relaxation.
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| 2. |
- Zhang, Jin-Yan, et al.
(författare)
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Dimethylsulfoxide-soluble Smoking Particles and Nicotine Affect Vascular Contractibility
- 2009
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Ingår i: Archives of Pharmacal Research. - : Springer Science and Business Media LLC. - 1976-3786 .- 0253-6269. ; 32:10, s. 1475-1481
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Tidskriftsartikel (refereegranskat)abstract
- The aim is to study the effect of dimethylsulfoxide-soluble smoking particles (DSP) and nicotine on the contractility of rat mesenteric artery. The superior mesenteric artery segments were cultured with DSP or nicotine for 24 h. The vascular contractibility was recorded with myograph system. DSP 0.4 mL/L and nicotine 0.48 and 0.96 mg/L shifted the concentration-contractile curves induced by sarafotoxin 6c, a selective agonist for ETB receptor toward the left with increased E-max. DSP 0.4 mL/L and nicotine 0.96 mg/L shifted ETA receptor-mediated the concentration-contractile curves toward the left with increased E-max. However, nicotine 0.06 mg/L which is the equivalent concentration of nicotine in DSP 0.4 mL/L did not affect the curves and the E-max mediated with ETA receptor and ETB receptor. DSP 0.2 and 0.4 mL/L shifted the concentration-contractile curves induced by noradrenaline toward the right with decreased E-max. Neither did nicotine 0.06 and 0.96 mg/L. Both DSP and nicotine shifted the concentration-contractile curves induced by 5-hydroxytryptamine (5-HT) toward the right parallely. DSP changed the phenotypes towards an increased efficacy of ETA receptor and ETB receptor, and a reduced efficacy of 5-HT receptor and alpha-adrenocceptor. The effects of DSP on ETB receptor, ETA receptor and alpha-adrenocceptor were independent of nicotine. The effect on 5-HT receptor was responsible to nicotine.
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| 3. |
- Lei, Ying, et al.
(författare)
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The Raf-1 inhibitor GW5074 and dexamethasone suppress sidestream smoke-induced airway hyperresponsiveness in mice
- 2008
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Ingår i: Respiratory Research. - : Springer Science and Business Media LLC. - 1465-9921 .- 1465-993X. ; 9
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Tidskriftsartikel (refereegranskat)abstract
- Background: Sidestream smoke is closely associated with airway inflammation and hyperreactivity. The present study was designed to investigate if the Raf-1 inhibitor GW5074 and the anti-inflammatory drug dexamethasone suppress airway hyperreactivity in a mouse model of sidestream smoke exposure. Methods: Mice were repeatedly exposed to smoke from four cigarettes each day for four weeks. After the first week of the smoke exposure, the mice received either dexamethasone intraperitoneally every other day or GW5074 intraperitoneally every day for three weeks. The tone of the tracheal ring segments was recorded with a myograph system and concentration-response curves were obtained by cumulative administration of agonists. Histopathology was examined by light microscopy. Results: Four weeks of exposure to cigarette smoke significantly increased the mouse airway contractile response to carbachol, endothelin-1 and potassium. Intraperitoneal administration of GW5074 or dexamethasone significantly suppressed the enhanced airway contractile responses, while airway epithelium-dependent relaxation was not affected. In addition, the smoke-induced infiltration of inflammatory cells and mucous gland hypertrophy were attenuated by the administration of GW5074 or dexamethasone. Conclusion: Sidestream smoke induces airway contractile hyperresponsiveness. Inhibition of Raf-1 activity and airway inflammation suppresses smoking-associated airway hyperresponsiveness.
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