Effects of histamine and nitric oxide synthase inhibition on plasma levels of von Willebrand factor antigen

Jilma, Bernd; Pernerstorfer, Thomas; Dirnberger, Eva; Stohlawetz, Petra; Schmetterer, Leopold; Singer, Ernst A.; Grasseli, Ursula; Eichler, Hans‐Georg; Kapiotis, Stylianos

doi:10.1016/s0022-2143(98)90157-3

Cited by 24 publications

(20 citation statements)

References 24 publications

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“…VWF can be produced and released by endothelial cells by a variety of stimuli in vitro and in vivo such as hypoxia, 15 inflammatory cytokines, 16 thrombin, 17 leukocyte elastase, 18 histamine, 4 endotoxin, 19 exercise, 20 adrenaline, 21 and especially vasopressin. 22 Indeed, patients with von Willebrand disease are effectively treated with desmopressin, the synthetic analog of vasopressin, to raise their VWF levels.…”

Section: Plasma and Subendothelial Vwfmentioning

confidence: 99%

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Von Willebrand Factor in Cardiovascular Disease

2008

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Abstract-von Willebrand factor (VWF) plays a pivotal role in platelet adhesion and aggregation at sites of high shear rates (eg, in coronary arteries that have stenotic or ruptured atherosclerotic plaque lesions). Numerous studies have investigated the relationship between VWF plasma levels and thromboembolic cardiovascular events. In contrast to the rather weak association in the general population, in patients with preexisting vascular disease, VWF is significantly predictive for adverse cardiac events, including death. Likewise, VWF typically rises during the course of acute coronary syndrome, and the extent of this VWF release is an independent predictor of adverse clinical outcome in these patients. Key Words: coronary disease Ⅲ myocardial infarction Ⅲ platelets Ⅲ thrombosis Ⅲ von Willebrand factor F or Ͼ150 years, it has been known that alterations in blood flow, vascular wall, and blood components, the so-called Virchow's triad, 1 may progressively lead to thrombus formation. Yet, a more complete understanding of the complex interactions among the vascular endothelium, platelet adhesion, activation, aggregation, and clotting factor activation involved in this process is still emerging from contemporary research.Under physiological conditions, the vascular endothelium produces many substances that contribute importantly to hemostasis, fibrinolysis, and regulation of vessel tone and permeability. One such substance is the multimeric glycoprotein von Willebrand factor (VWF), which is produced almost exclusively by endothelial cells. 2 Plasma levels of VWF are raised in different states of endothelial damage and have therefore been proposed as useful markers of endothelial dysfunction. 3 Along this line, blockade of nitric oxide enhances the stimulated release of VWF in humans. 4,5 Furthermore, VWF plays a crucial role in platelet adhesion and aggregation under high shear conditions. 6 Finally, VWF supports the third component of Virchow's triad, clotting factor activation, by acting as a carrier protein and stabilizer for factor VIII. 7 Almost all acute coronary syndromes (ACS) result from thrombus formation in preexisting coronary atherosclerosis. As a result of plaque rupture and exposure of prothrombotic subendothelial matrix, local thrombus formation occurs, which subsequently leads to coronary artery occlusion and acute myocardial infarction (AMI). The presence of VWF has been shown to play a pivotal role in platelet aggregation at sites of high shear, eg, at the sites of lesions in the coronary arteries. 8 Accordingly, VWF is a well-characterized marker of cardiovascular risk, and VWF plasma levels are increased in patients with ACS. 9 Considering the central role of VWF in thrombogenesis, therapies that specifically inhibit VWF are of particular interest as potential new antiplatelet drugs.

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Section: Plasma and Subendothelial Vwfmentioning

confidence: 99%

“…3 Along this line, blockade of nitric oxide enhances the stimulated release of VWF in humans. 4,5 Furthermore, VWF plays a crucial role in platelet adhesion and aggregation under high shear conditions. 6 Finally, VWF supports the third component of Virchow's triad, clotting factor activation, by acting as a carrier protein and stabilizer for factor VIII.…”

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confidence: 99%

Von Willebrand Factor in Cardiovascular Disease

2008

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“…Thus, the regulation of endothelial exocytosis has been extensively studied. The regulation of WPB exocytosis involves the activation of canonical pathways mediated by second messengers, such as calcium and cAMP [3,4], and the induction of a negative pathway executed by nitric oxide (NO), which inhibits the exocytosis of WPBs by the S-nitrosylation of N-ethylmaleimide-sensitive factor (NSF), a component of the membrane fusion and exocytotic machinery [5,6]. So far, however, the vast majority of our knowledge on the regulation of WPB exocytosis has been obtained from the studies conducted with chemical agonists, such as thrombin, histamine and VEGF.…”

Section: Introductionmentioning

confidence: 99%

Hypertensive stretch regulates endothelial exocytosis of Weibel-Palade bodies through VEGF receptor 2 signaling pathways

Xiong

Han

et al. 2013

Cell Res

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Regulated endothelial exocytosis of Weibel-Palade bodies (WPBs), the first stage in leukocyte trafficking, plays a pivotal role in inflammation and injury. Acute mechanical stretch has been closely associated with vascular inflammation, although the precise mechanism is unknown. Here, we show that hypertensive stretch regulates the exocytosis of WPBs of endothelial cells (ECs) through VEGF receptor 2 (VEGFR2) signaling pathways. Stretch triggers a rapid release (within minutes) of von Willebrand factor and interleukin-8 from WPBs in cultured human ECs, promoting the interaction between leukocytes and ECs through the translocation of P-selectin to the cell membrane. We further show that hypertensive stretch significantly induces P-selectin translocation of intact ECs and enhances leukocyte adhesion both ex vivo and in vivo. Stretch-induced endothelial exocytosis is mediated via a VEGFR2/PLCγ1/calcium pathway. Interestingly, stretch also induces a negative feedback via a VEGFR2/Akt/nitric oxide pathway. Such dual effects are confirmed using pharmacological and genetic approaches in carotid artery segments, as well as in acute hypertensive mouse models. These studies reveal mechanical stretch as a potent agonist for endothelial exocytosis, which is modulated by VEGFR2 signaling. Thus, VEGFR2 signaling pathways may represent novel therapeutic targets in limiting hypertensive stretch-related inflammation.

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“…The fact that ACSs patients had lower NO and H 2 O 2 levels may be brought into connection with vWf levels, since reactive oxygen species and NO are involved in the regulation of vWf release. It was previously suggested that the blockade of nitric oxide enhances the stimulated release of vWf in humans [47, 48], that is, NO exerts inhibitory effects on vWf release [5]. So, is thought for H 2 O 2 [5].…”

Section: Discussionmentioning

confidence: 99%

von Willebrand Factor and Oxidative Stress Parameters in Acute Coronary Syndromes

Koprivica¹,

Djordjevic

Vuletić

et al. 2011

Oxidative Medicine and Cellular Longevity

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Considering the role of von Willebrand factor (vWf) in hemostasis, and the role of oxidative stress in the development of endothelial dysfunction and atherosclerotic disease, the aim of our study was to investigate the relationship between vWf, parameters of oxidative stress and different types of acute coronary syndromes (ACS). Levels of vWf activity (vWfAct), vWf antigen (vWfAg), nitric oxide (estimated through nitrites–NO2 −), superoxide anion radical (O2 −), hydrogen peroxide (H2O2), index of lipid peroxidation (estimated through thiobarbituric acid reactive substances–TBARS), superoxide dismutase (SOD) and catalase (CAT) activity of 115 patients were compared with those of 40 healthy controls. ACS patients had significantly higher vWfAct and vWfAg levels, as well as TBARS levels, while their levels of NO2 −, H2O2, SOD and CAT activities were lower than controls'. vWfAg showed high specificity and sensitivity as a test to reveal healthy or diseased subjects. Multivariant logistic regression marked only vWfAg and TBARS as parameters that were under independent effect of ACS type. The results of our study support the implementation of vWf in clinical rutine and into therapeutic targets, and suggest that ACS patients are in need of antioxidant supplementation to improve their impaired antioxidant defence.

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Effects of histamine and nitric oxide synthase inhibition on plasma levels of von Willebrand factor antigen

Cited by 24 publications

References 24 publications

Von Willebrand Factor in Cardiovascular Disease

Von Willebrand Factor in Cardiovascular Disease

Hypertensive stretch regulates endothelial exocytosis of Weibel-Palade bodies through VEGF receptor 2 signaling pathways

von Willebrand Factor and Oxidative Stress Parameters in Acute Coronary Syndromes

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