检索结果-南通市图书馆

维普期刊数据库

Hypoxia,vascular smooth muscles and endothelium

在线全文

学校读者我要写书评

暂无评论

Acta Pharmaceutica Sinica B 2013年第1期3卷 1-7页

作者： Calvin K.Chan paul m.vanhoutte Department of Pharmacology and Pharmacy University of Hong KongHong KongChina Department of BIN Fusion Technology Chonbuk National UniversityJeonjuSouth Korea

Hypoxia,or the lack of oxygen,has multiple impacts on the vascular *** major molecular sensors for hypoxia at the cellular level are hypoxia inducible factor and heme *** also acts on the vasculature directly conveying its damaging effects through disruption of the control of vascular tone,particularly in the coronary circulation,enhancement of inflammatory responses and activation of coagulation *** effects could be particularly detrimental under pathological conditions such as obstructive sleep apnea and other breathing disorders.

关键词： Coronary circulation Contractions Hypoxia Endothelium

rho家族的小分子量G蛋白介导缓激肽引起的猪冠状动脉松弛(英文)

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Acta Pharmacologica Sinica 2003年第11期24卷 8-14+110页

作者： Toshiro SHIBANO,paul m vanhoutte Center for Experimental Therapeutics Baylor College of medicine One Baylor Plaza Houston TX 77030 USA Department of Pharmacology University of Hong Kong Hong Kong China

AIm: To determine whether or not low molecular G-proteins are involved in the endothelium-dependent relaxations to bradykinin. mETHODS: The effects of botulinum ADP-ribosyltranferase C3 were studied in porcine coronaryarteries and endothelial cells. RESULTS: Incubation of membrane fractions isolated from endothelial cells with the enzyme and32P-NAD resulted in the ribosylation of the proteins with molecular weight of 24-25 kDa. Radio labelling of these proteins was suppressed in the presence of guanosine 5'-O-（3-thiotriphosphate）（GTP-γS）, a hydrolysis-resistant analog of GTP. In the isolated arteries, ADP-ribosyltransferase C3 attenuated the relaxations to bradykinin during contractions with prostaglandin F2ain the presence of tween 80（non ionic detergent）, but not in the absence of tween 80. CONCLUSION: Low molecular weight G-proteins of the Rho family contribute to the mechanism of relaxation induced by bradykinin.

关键词：缓激肽内皮 G蛋白一氧化氮

前列腺素而非一氧化氮是鳟主动脉内皮细胞舒血管因子(英文)

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Acta Pharmacologica Sinica 2000年第10期21卷 10-15页

作者： Virginia m mILLER,paul m vanhoutte Departments of Surgery and Physiology and Bio-physics mayo Clinic and Foundation 200 First Street SW Rochester mN 55905 USA Institut De Recherches Internationales Servier 6 place des Pléiades 92415 Courbevoie Cedex France

AIm:To identify the type of prostanoids produced by endothelial cells of trout aorta and to determine whether or not the smooth muscle responds to nitric oxide. mETHODS:Ventral aortas, with and without endotheli-um from rainbow trout (S gairdneri), were incubated in a buffered salt solution. RESULTS:Addition of the calcium ionophore A23187 caused a significant increase in prostaglandin E's and a consistent increase in the stable metabolite of prostacyclin (6-keto-prostaglandin F1a) in the incubation media only when the endothelium was present. This production was inhibited by methylene blue (10umol/L). In rings of trout aorta without endothelium suspended for the measurement of isometric force in organ chambers,prostacyclin and prostaglandin E1 but not prostaglandin E2 caused concentration-dependent decreases in tension when the rings were contracted with acetyl-choline. The smooth muscle did not relax to nitric oxide but did so to sodium nitroprusside. Relaxations to the latter nitrovasodilator were no

关键词：乙酰胆碱钙离子载体牛蛙亚甲蓝

自发性高血压大鼠主动脉对前列腺素H_2反应的增加先于前列腺素H合酶1表达的变化(英文)

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

中国药理学报 1999年第12期20卷 1087-1092页

作者： Tong GE paul m vanhoutte Chantal m BOULANGER Center for Experimental Therapeutics Baylor College of Medicine Houston TX 77030 USAIRIS 6 Place des Pleiades 92415 Courbevoie cdex FranceCenter for Experimental Therapeutics Baylor College of Medicine Houston TX 77030 USA

AIm: To determine the expression of PGH synthase-1and the sensitivity of vascular smooth muscle to PGH_2in the aorta from the SHR at an age when noendothelium-dependent contractions to acetylcholine areobserved under control conditions. mETHODS: Allexperiments were performed in parallel on aortas from20-wk-old SHR and Wistar-Kyoto normotensive rats(WKY). Rings, with or without endothelium, weresuspended in conventional organ chambers for therecording of changes in isometric force. Theexpression of PGH Synthase-1 was evaluated by

关键词：乙酰胆碱前列腺素过氧化物合酶 PCH

转换酶抑制剂培哚普利拉非激肽酶依赖性地加强由激肽引起的内皮依赖性血管松弛(英文)

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Acta Pharmacologica Sinica 2002年第3期23卷 15-19页

作者： Jean Vivien mOmBOULI,Kevin D BALLARD,paul m vanhoutte University of marien Ngouabi Brazzaville Republic of Congo Center for Experimental Therapeutics Baylor College of medicine Houston Texas USA Institut de Recherches Internationales Servier 92415 Courbevoie Cedex France

The present study examined whether or not the resistance to degradation of bradykinin analogs affects the kinin-potentiating action of the inhibitor of converting enzyme, perindoprilat. mETHODS: Hydrolysis of [Hyp3,Tyr(me)8]-bradykinin by ACE present in isolated canine coronary arteries was assessed by determination of peptide metabolites using electrospray mass spectrometry, and compared to that of bradykinin. Contractions and relaxations of isolated rings of coronary arteries, with and without endothelium, were recorded as changes in isometric force. RESULTS: After a 30 min incubation, most of the bradykinin was degraded by the arteries, while less than 10 % of [Hyp3 Tyr(me)8]-bradykinin was hydrolysed. In organ chambers, [Hyp3, Tyr(me)8]-bradykinin like bradykinin caused relaxations of isolated canine coronary arteries with endothelium that could be attributed to both NO and endothelium-derived hyperpolarizing factor (EDHF). Perindoprilat caused a comparable leftward shift in the concentration-relaxa

关键词：缓激肽受体一氧化氮内皮血管紧张素转换酶抑制药肽基-二肽酶A

内皮素-1促进猪冠状动脉再生内皮释放内皮衍生内过氧化物和血栓素A_2(英文)

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

中国药理学报 1999年第10期20卷 872-878页

作者： Seung-Jung PARK John J LEE paul m vanhoutte Center for Experimental Therapeutics Department of Medicine Baylor College of Medicine One Baylor Plaza Houston TX 77030 USACenter for Experimental Therapeutics Department of Medicine Baylor College of Medicine One Baylor Plaza Houston TX 77030 USACenter for Experimental Therapeutics Department of Medicine Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA

AIm: To determine the role of endothelium-derivedcontracting factor (EDCF) in the response toendothelin-1 in arteries with regenerated ***: Rings of porcine coronary arteries, withand without endothelium of previously deendothelializedleft anterior descending coronary arteries and native leftcircumflex coronary arteries, were suspended inconventional organ chambers for the measurement ofisometric force. RESULTS: In quiescent rings of thepreviously deendothelialized left anterior

关键词：血管内皮药理冠状血管内皮素-1 吲哚美辛

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

一氧化氮研究三十年:自优而劣（英文）

中国药理学与毒理学杂志 2016年第10期30卷 999-1000页

作者： paul m.vanhoutte State Key Laboratory of Pharmaceutical Biotechnology and Department of Pharmacology and Pharmacy Li Ka Shing Faculty of MedicineUniversity of Hong KongHong KongChina

In the last thirty years,it became over whelmingly apparent that the endothelium releases relaxing factors(EDRF),which diffuse to the underlying vascular smooth muscle cells and elicit endothelium-dependent *** best characterized EDRF is nitric oxide(NO)formed by endothelial NO synthase(e NOS).In the vascular smooth muscle cells,NO stimulates soluble guanylate cyclase which normally produces cyclic *** release by e NOS can be augmented by increases in shear stress or by activation of endothelial cell membrane receptors(*** response toα2-adrenergic agonists,serotonin,vasopressin,adenosine diphosphate and bradykinin).The ability of the endothelial cell to release NO can be up-regulated by estrogens,repeated increases in blood flow,exercise,diet(ω3-unsaturated fatty acids,polyphenols),and down-regulated by oxidative stress and increased presence of oxidized low density lipoproteins(LDL).The bioavailability of NO is curtailed by aging,smoking,environmental pollution or obesity and in hypertension and *** addition to lesser direct relaxation of the underlying vascular smooth muscle,a decreased release of NO also permits the production of vasoconstrictor prostanoids and/or *** endothelium-dependent relaxations can also be due to unresponsiveness of the vascular smooth muscle to ***,in coronary arteries,hypoxia and certain quinonescause acute augmentations of vasoconstrictor responses that depend on the presence of NO and the biased activation of soluble guanylate cyclase which produces cyclic ImP rather than cyclic *** hypoxia is implicated in exaggerated vasoconstrictions observed in coronary artery disease,the emerging role of this non-canonical cyclic nucleotide may help identifying novel therapeutic targets.

关键词： NOS GmP

维普期刊数据库

Endothelial dysfunction:EDCF revisited

在线全文

学校读者我要写书评

暂无评论

Endothelial dysfunction:EDCF revisited

SIRT1 and AmPK:the Seesaw Effect in Regulating Endothelial Sene-scence

两岸三地药理学与临床药理学术会议

作者： paul m vanhoutte Department of Pharmacology University of Hong Kong

Endothelial cells can initiate contraction(constriction)of the vascular smooth muscle cells that surround *** endothelium-dependent,acute increases in contractile tone can be due to the withdraw- al of the production of nitric oxide,to the production of vasoconstrictor peptides(angiotensinⅡ,endothelin- 1),to the formation of oxygen-derived free radicals(superoxide anions)and/or the release of vasoconstrictor metabolites of arachidonic *** latter have been termed endothelium-derived contracting factor(EDCF) as they can contribute to moment-to-moment changes in contractile activity of the underlying vascular smooth muscle *** judge from animal experiments,EDCF-mediated responses are exacerbated when the production of nitric oxide is impaired as well as by aging,spontaneous hypertension and *** judge from human studies,they contribute to the blunting of endothelium-dependent vasodilatations in aged sub- jects and essential hypertensive *** EDCF causes vasoconstriction by activation of the TP-recep- tors on the vascular smooth muscle cells,selective antagonists at these receptors prevent endothelium-depen- dent contractions,and curtail the endothelial dysfunction in hypertension and diabetes.

关键词： EDCF TP-receptors nitric oxide

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

SIRT1 and AMPK:the Seesaw Effect in Regulating Endothelial S...