標(biāo)題: Titlebook: Endothelial Function in Hypertension; David Webb,Patrick Vallance Conference proceedings 1997 Springer-Verlag Berlin Heidelberg 1997 ather [打印本頁(yè)] 作者: 鳴叫大步走 時(shí)間: 2025-3-21 17:57
書(shū)目名稱Endothelial Function in Hypertension影響因子(影響力)
書(shū)目名稱Endothelial Function in Hypertension影響因子(影響力)學(xué)科排名
書(shū)目名稱Endothelial Function in Hypertension網(wǎng)絡(luò)公開(kāi)度
書(shū)目名稱Endothelial Function in Hypertension網(wǎng)絡(luò)公開(kāi)度學(xué)科排名
書(shū)目名稱Endothelial Function in Hypertension被引頻次
書(shū)目名稱Endothelial Function in Hypertension被引頻次學(xué)科排名
書(shū)目名稱Endothelial Function in Hypertension年度引用
書(shū)目名稱Endothelial Function in Hypertension年度引用學(xué)科排名
書(shū)目名稱Endothelial Function in Hypertension讀者反饋
書(shū)目名稱Endothelial Function in Hypertension讀者反饋學(xué)科排名
作者: regale 時(shí)間: 2025-3-21 23:20
Conference proceedings 1997 in these conditions. Here, a synthesis of the current understanding of endothelial dysfunction in hypertension and related disorders - and future therapeutic prospects - has been drawn together by a series of internationally recognised leaders in the field.作者: 施加 時(shí)間: 2025-3-22 02:04 作者: 權(quán)宜之計(jì) 時(shí)間: 2025-3-22 07:24
Erkenntnisinteresse und Herangehensweise,s may occur by interaction with superoxide. This brief review summarizes current understanding of these “other factors” which contribute to abnormal endothelial cell control of vascular tone in vascular disease states.作者: Allodynia 時(shí)間: 2025-3-22 12:11
https://doi.org/10.1007/978-3-531-91647-7 associated with CHF may be decreased by interrupting the ET system thus supporting the inhibition of ET as a treatment strategy. Thus, ET emerges as both a marker and mediator of CHF as well as a key target in the therapeutics for this important cardiovascular disease.作者: 打折 時(shí)間: 2025-3-22 13:37
Other Factors in Endothelial Cell Dysfunction in Hypertension and Diabetes,s may occur by interaction with superoxide. This brief review summarizes current understanding of these “other factors” which contribute to abnormal endothelial cell control of vascular tone in vascular disease states.作者: 打折 時(shí)間: 2025-3-22 18:01 作者: Ergots 時(shí)間: 2025-3-23 00:04
Steuerung als Element von Schulentwicklung, endothelial cells all have the capacity to affect cardiovascular behaviour through generation of NO. Here we discuss the role of NO in the maintenance of normal blood pressure and flow, and describe the significance of the changes that occur in experimental and clinical hypertension. We have reviewed the role of NO in hypotension elsewhere [3].作者: 消音器 時(shí)間: 2025-3-23 05:08 作者: 無(wú)動(dòng)于衷 時(shí)間: 2025-3-23 08:23
Nitric Oxide and Hypertension: Physiology and Pathophysiology, endothelial cells all have the capacity to affect cardiovascular behaviour through generation of NO. Here we discuss the role of NO in the maintenance of normal blood pressure and flow, and describe the significance of the changes that occur in experimental and clinical hypertension. We have reviewed the role of NO in hypotension elsewhere [3].作者: Nonflammable 時(shí)間: 2025-3-23 13:44
https://doi.org/10.1007/978-3-658-33062-0cell adhesion molecule-1 and monocyte chemotactic protein-1..Enhancement of endogenous NO activity may be a new therapeutic strategy for preventing the progression of atherosclerotic vascular disease, restenosis, and thrombosis.作者: Cpr951 時(shí)間: 2025-3-23 15:43 作者: 粗糙濫制 時(shí)間: 2025-3-23 18:33
Endothelial Function in Hypertension: Role of Nitric Oxide,r NO synthase. In human hypertension, pharmacological experiments reveal an impaired NO dilator mechanism. In pulmonary hypertension, the use of NO gas inhalation has been proposed as a future therapy for this condition. This chapter reviews the evidence, concentrating on the evidence from animal mo作者: 謙卑 時(shí)間: 2025-3-23 22:43
Endothelial Factors and Myocardial Function,ous to endothelium-dependent regulation of vascular tone. In bioassay studies using cultured ventricular endocardial endothelial cells and isolated papillary muscle preparations, Shah and colleagues (Smith et al. 1991) demonstrated that these effects were mediated by the release of diffusible factor作者: 性上癮 時(shí)間: 2025-3-24 06:09
Vascular Biology of the Endothelin System,paired cysteine amino acid residues and all of which are formed through the same processing pathway (Fig. 2). Their respective precursor peptides share high sequence homology but are encoded by distinct genes [7]. It is also clear [8] that the endothelin isopeptides share remarkable structural simil作者: 蘆筍 時(shí)間: 2025-3-24 10:20 作者: overrule 時(shí)間: 2025-3-24 11:58
Endothelin in Hypertension: A Role in Vascular Hypertrophy?,vascular hypertrophy in these experimental models of hypertension, whereas it has no effect on SHR. The latter do not overexpress endothelin in blood vessels. In some severe hypertensive patients there is overexpression of endothelin-1 in endothelium of small arteries. These results suggest that end作者: –DOX 時(shí)間: 2025-3-24 18:45 作者: Charade 時(shí)間: 2025-3-24 21:18
https://doi.org/10.1007/978-3-322-95122-9r NO synthase. In human hypertension, pharmacological experiments reveal an impaired NO dilator mechanism. In pulmonary hypertension, the use of NO gas inhalation has been proposed as a future therapy for this condition. This chapter reviews the evidence, concentrating on the evidence from animal mo作者: Self-Help-Group 時(shí)間: 2025-3-24 23:22 作者: reaching 時(shí)間: 2025-3-25 04:20 作者: COLIC 時(shí)間: 2025-3-25 08:43 作者: 表被動(dòng) 時(shí)間: 2025-3-25 13:32 作者: Infinitesimal 時(shí)間: 2025-3-25 18:35 作者: 草率男 時(shí)間: 2025-3-25 23:24
Nitric Oxide and Hypertension: Physiology and Pathophysiology,n of endothelium-dependent relaxation and the existence of the endothelium-derived relaxing factor (EDRF) were described [1]. Seven years later EDRF was identified as an inorganic gas, NO [2]. Now it is clear that neurones, smooth muscle cells, cardiac myocytes, white cells and platelets, as well as作者: 劇本 時(shí)間: 2025-3-26 04:03 作者: Conflict 時(shí)間: 2025-3-26 05:41
Endothelial Alterations in Atherosclerosis: The Role of Nitric Oxide,ay be due to reduced NO synthesis and/or increased degradation. A reduction in NO activity favors vasoconstriction, platelet adherence and aggregation, monocyte adherence, and generation of superoxide anion. NO affects these processes by cyclic GMP-dependent and cyclic GMP-independent pathways. By r作者: GLUT 時(shí)間: 2025-3-26 10:55 作者: GENRE 時(shí)間: 2025-3-26 12:56
Endothelial Factors and Myocardial Function,ells lining the inner surfaces of the cardiac chambers. It is now recognised that these cardiac endothelial cells influence myocardial function through the paracrine release of a variety of diffusible substances (Shah 1996). The initial suggestion that endothelial cells influence myocardial function作者: BRIDE 時(shí)間: 2025-3-26 18:32
Vascular Biology of the Endothelin System,he vascular relaxation to acetylcholine [2] and the subsequent identification of this factor as nitric oxide [3]. An additional important stimulus to the discovery of endothelin was the recognition that endothelial cells in culture generate and release a polypeptide vasoconstrictor factor into the b作者: Gossamer 時(shí)間: 2025-3-26 22:37
Endothelin Antagonists: Novel Treatments for Hypertension?,erived from the vascular endothelium (Yanagisawa et al. 1988). When administered intravenously in experimental animals or man ET-1 produces long-lasting increases in blood pressure (Yanagisawa et al.1988; Clarke et al.1989; Vierhapper et al.1990). ET-1 can also modulate blood pressure by potentiatio作者: 你正派 時(shí)間: 2025-3-27 03:32
Endothelin in Hypertension: A Role in Vascular Hypertrophy?,ts. Endothelin-1 is the main endothelin produced by the endothelium. Plasma levels of immunoreactive endothelin are normal or only slightly increased in experimental or human hypertension. The responsiveness of blood vessels to endothelin-1 is normal or attenuated in experimental and human hypertens作者: Feedback 時(shí)間: 2025-3-27 09:11
Endothelin in Congestive Heart Failure: Pathophysiology and Therapeutic Implications,mechanism of activation of ET in CHF probably is multifactorial and includes stimulation by factors such as Angiotensin II and tissue hypoxia. The functional significance of ET activation in CHF is currently being elucidated by the use of potent ET receptor antagonists. Such studies support the conc作者: 流出 時(shí)間: 2025-3-27 10:48 作者: Confirm 時(shí)間: 2025-3-27 16:24
https://doi.org/10.1007/978-3-642-60811-7atherosclerosis; blood pressure; cardiovascular; endothelin; heart; heart failure; hypertension; physiology作者: Expiration 時(shí)間: 2025-3-27 20:18
Steuerung als Element von Schulentwicklung,n of endothelium-dependent relaxation and the existence of the endothelium-derived relaxing factor (EDRF) were described [1]. Seven years later EDRF was identified as an inorganic gas, NO [2]. Now it is clear that neurones, smooth muscle cells, cardiac myocytes, white cells and platelets, as well as作者: 專橫 時(shí)間: 2025-3-28 01:50
https://doi.org/10.1007/978-3-322-95122-9whether its production is or not affected in hypertension has been very controversial. Recent research work is showing the existence of profound differences in the role of NO in hypertension. This role seems to vary depending on the class of hypertension. In spontaneous and renovascular hypertension作者: 冷漠 時(shí)間: 2025-3-28 03:15 作者: 臨時(shí)抱佛腳 時(shí)間: 2025-3-28 06:29
Erkenntnisinteresse und Herangehensweise,sease processes, simply by alterations in the quantity of nitric oxide released from endothelial cells (Cohen 1995). It is now clear that superoxide anion inactivates nitric oxide, that superoxide anion levels are a major determinant of nitric oxide activity and endothelial cell function, and that d作者: FLAG 時(shí)間: 2025-3-28 10:44
https://doi.org/10.1007/978-3-658-18151-2ells lining the inner surfaces of the cardiac chambers. It is now recognised that these cardiac endothelial cells influence myocardial function through the paracrine release of a variety of diffusible substances (Shah 1996). The initial suggestion that endothelial cells influence myocardial function作者: Orgasm 時(shí)間: 2025-3-28 15:58
Jugend, Studium und erste Praktikantenjahre,he vascular relaxation to acetylcholine [2] and the subsequent identification of this factor as nitric oxide [3]. An additional important stimulus to the discovery of endothelin was the recognition that endothelial cells in culture generate and release a polypeptide vasoconstrictor factor into the b作者: Osmosis 時(shí)間: 2025-3-28 20:45 作者: monochromatic 時(shí)間: 2025-3-29 02:48 作者: 高腳酒杯 時(shí)間: 2025-3-29 04:27
https://doi.org/10.1007/978-3-531-91647-7mechanism of activation of ET in CHF probably is multifactorial and includes stimulation by factors such as Angiotensin II and tissue hypoxia. The functional significance of ET activation in CHF is currently being elucidated by the use of potent ET receptor antagonists. Such studies support the conc
