Role of ETBand B2receptors in theex vivoplatelet inhibitory properties of endothelin and bradykinin in the mouse

Labonté, Julie; Brochu, Isabelle; Honoré, Jean-Claude; D’Orléans-Juste, Pedro

doi:10.1038/sj.bjp.0703880

Cited by 19 publications

(18 citation statements)

References 28 publications

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“…Through these mechanisms, BK prevents or reduces the occurrence of thrombosis and may inhibit haemostatis, [54][55][56] contributing to improved tissue perfusion. Some of the proteins involved in, stimulated by, or associated with thrombosis include fibrinogen, D-dimer, 8 vWF, 9 and TAT complex 10 ( Figure 2).…”

Section: Thrombosismentioning

confidence: 99%

Potential Vascular Mechanisms of Ramipril Induced Increases in Walking Ability in Patients With Intermittent Claudication

Ahimastos

Latouche

Natoli

et al. 2014

Circulation Research

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Rationale: We recently reported that ramipril more than doubled maximum walking times in patients with peripheral artery disease with intermittent claudication. Objective: Our aim was to conduct exploratory analyses of the effects of ramipril therapy on circulating biomarkers of angiogenesis/arteriogenesis, thrombosis, inflammation, and leukocyte adhesion in patients with intermittent claudication. Methods and Results: One hundred sixty-five patients with intermittent claudication (mean, 65.3 [SD, 6.7] years) were administered ramipril 10 mg per day (n=82) or matching placebo (n=83) for 24 weeks in a randomized, double-blind study. Plasma biomarkers of angiogenesis/arteriogenesis (vascular endothelial growth factor-A, fibroblast growth factor-2), thrombosis (D-dimer, von Willebrand factor, thrombin-antithrombin III), inflammation (high-sensitivity C-reactive protein, osteopontin), and leukocyte adhesion (soluble vascular cell adhesion molecule-1, soluble intracellular adhesion molecule-1) were measured at baseline and 24 weeks. Relative to placebo, ramipril was associated with increases in vascular endothelial growth factor-A by 38% (95% confidence interval [CI], 34%–42%) and fibroblast growth factor-2 by 64% (95% CI, 44–85%; P <0.001 for both), and reductions in D-dimer by 24% (95% CI, −30% to −18%), von Willebrand factor by 22% (95% CI, −35% to −9%), thrombin-antithrombin III by 16% (95% CI, −19% to −13%), high-sensitivity C-reactive protein by 13% (95% CI, −14% to −9%), osteopontin by 12% (95% CI, −14% to −10%), soluble vascular cell adhesion molecule-1 by 14% (95% CI, −18% to −10%), and soluble intracellular adhesion molecule-1 by 15% (95% CI, −17% to −13%; all P <0.001). With the exception of von Willebrand factor, all the above changes correlated significantly with the change in maximum walking time ( P =0.02−0.001) in the group treated with ramipril. Conclusions: Ramipril is associated with an increase in the biomarkers of angiogenesis/arteriogenesis and reduction in the markers of thrombosis, inflammation, and leukocyte adhesion. This study informs strategies to improve mobility in patients with intermittent claudication. Clinical Trial Registration Information: URL: http://clinicaltrials.gov . Unique identifier: NCT00681226.

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Section: Thrombosismentioning

confidence: 99%

Potential Vascular Mechanisms of Ramipril Induced Increases in Walking Ability in Patients With Intermittent Claudication

Ahimastos

Latouche

Natoli

et al. 2014

Circulation Research

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“…46 Both of these endothelial-derived factors modulate platelet-vessel wall interactions, inhibit aggregation, and promote disaggregation in vitro and in animal models. 47 Studies in bradykinin B 2 receptor knockout mice indicate that the anti-aggregatory effects of bradykinin occur via the B 2 receptor, 48 although bradykinin and its metabolite BK1-5 can also inhibit thrombin-induced platelet aggregation via interactions with protease-activated receptor 1. 13,49 Bradykinin causes vasodilation via the B 2 receptor-mediated release of prostacyclin, NO, and endothelium-derived hyperpolarizing factor; 46 however, the lack of effect of HOE-140 on the hypotensive response to hemodialysis suggests that endogenous bradykinin does not substantially contribute to the hemodynamic response to hemodialysis.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Bradykinin Contributes to Increased Plasminogen Activator Inhibitor 1 Antigen following Hemodialysis

Marney¹,

Ma²,

Luther

et al. 2009

Journal of the American Society of Nephrology

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Oxidative stress and inflammation predict cardiovascular events in chronic hemodialysis patients. Hemodialysis activates the kallikrein-kinin system, increasing bradykinin. Bradykinin promotes inflammation but also stimulates endothelial release of tissue-plasminogen activator and inhibits platelet aggregation. Understanding the detrimental and beneficial effects of endogenous bradykinin during hemodialysis has implications for the treatment of cardiovascular disease in the hemodialysis population. To test the hypothesis that bradykinin contributes to the inflammatory and fibrinolytic responses to dialysis, we conducted a double-blind, randomized, placebo-controlled crossover study comparing the effect of the bradykinin B 2 receptor blocker HOE-140 with vehicle on markers of oxidative stress, inflammation, fibrinolysis, and coagulation in nine hemodialysis patients without coronary artery disease. Bradykinin receptor antagonism did not affect the mean arterial pressure or heart rate response to dialysis. Monocyte chemoattractant protein 1 (MCP-1) peaked postdialysis; HOE-140 blunted the increase in MCP-1 (5.9 Ϯ 5.9 versus 25.6 Ϯ 20.1 pg/ml, P ϭ 0.01). HOE-140 also abolished the increase in plasminogen activator inhibitor 1 (PAI-1) antigen observed at the end of dialysis. In contrast, HOE-140 significantly accentuated the effect of dialysis on F 2 -isoprostanes and P-selectin. Taken together, these results suggest that endogenous bradykinin contributes to increases in MCP-1 and PAI-1 antigen after hemodialysis via its B 2 receptor. Factors that increase the production of bradykinin or decrease its degradation may enhance the inflammatory response to hemodialysis.

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“…Primer pairs (5V -CAGCTCTGGAGAACTGCTG-3V and 5V -GTGTACTCAGTCTCCACAGA-3V ; ref. 24) were used in RT-PCR analysis to detect 36B4 mRNA (24). The RT-PCR DNA products were subcloned using a topoisomerase PCR system (Invitrogen, Carlsbad, CA) and sequenced by automated sequencing (SeqWright, Houston, TX) to verify the insert DNA.…”

Section: Introductionmentioning

confidence: 99%

Suppression of Prostate Tumor Cell Growth by Stromal Cell Prostaglandin D Synthase–Derived Products

Kim

Yang²,

Suraokar

et al. 2005

Cancer Research

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Stromal-epithelial interactions and the bioactive molecules produced by these interactions maintain tissue homeostasis and influence carcinogenesis. Bioactive prostaglandins produced by prostaglandin synthases and secreted by the prostate into seminal plasma are thought to support reproduction, but their endogenous effects on cancer formation remain unresolved. No studies to date have examined prostaglandin enzyme production or prostaglandin metabolism in normal prostate stromal cells. Our results show that lipocalin-type prostaglandin D synthase (L-PGDS) and prostaglandin D 2 (PGD 2 ) metabolites produced by normal prostate stromal cells inhibited tumor cell growth through a peroxisome proliferator-activated receptor ; (PPAR;)-dependent mechanism. Enzymatic products of stromal cell L-PGDS included high levels of PGD 2 and 15-deoxy-# 12,14 -PGD 2 but low levels of 15-deoxy-# 12,14 -prostaglandin J 2 . These PGD 2 metabolites activated the PPAR; ligand-binding domain and the peroxisome proliferator response element reporter systems. Thus, growth suppression of PPAR;-expressing tumor cells by PGD 2 metabolites in the prostate microenvironment is likely to be an endogenous mechanism involved in tumor suppression that potentially contributes to the indolence and long latency period of this disease. (Cancer Res 2005; 65(14): 6189-98)

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Role of ET_Band B₂receptors in theex vivoplatelet inhibitory properties of endothelin and bradykinin in the mouse

Cited by 19 publications

References 28 publications

Potential Vascular Mechanisms of Ramipril Induced Increases in Walking Ability in Patients With Intermittent Claudication

Potential Vascular Mechanisms of Ramipril Induced Increases in Walking Ability in Patients With Intermittent Claudication

Endogenous Bradykinin Contributes to Increased Plasminogen Activator Inhibitor 1 Antigen following Hemodialysis

Suppression of Prostate Tumor Cell Growth by Stromal Cell Prostaglandin D Synthase–Derived Products

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