Vasopressin acts on platelets to generate procoagulant activity

Tomasiak, Marian; Stelmach, Halina; Rusak, Tomasz; Ciborowski, Michał; Radziwon, Piotr

doi:10.1097/mbc.0b013e328309905d

Cited by 17 publications

(5 citation statements)

References 38 publications

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“…Vasopressin and the renin-angiotensin system are important after hemorrhage as they affect blood pressure and volume; however, they may also influence hemostatic competence. Vasopressin elevates the expression of phosphatidylserine on platelet surfaces and enhances thrombin generation [24] , and increases fibrinolysis by elevating plasma t-PA [25] . In the present study, however, vasopressin did not differ from baseline.…”

Section: Discussionmentioning

confidence: 99%

Platelet Activation after Presyncope by Lower Body Negative Pressure in Humans

et al. 2014

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Central hypovolemia elevates hemostatic activity which is essential for preventing exsanguination after trauma, but platelet activation to central hypovolemia has not been described. We hypothesized that central hypovolemia induced by lower body negative pressure (LBNP) activates platelets. Eight healthy subjects were exposed to progressive central hypovolemia by LBNP until presyncope. At baseline and 5 min after presyncope, hemostatic activity of venous blood was evaluated by flow cytometry, thrombelastography, and plasma markers of coagulation and fibrinolysis. Cell counts were also determined. Flow cytometry revealed that LBNP increased mean fluorescence intensity of PAC-1 by 1959±455 units (P<0.001) and percent of fluorescence-positive platelets by 27±18%-points (P = 0.013). Thrombelastography demonstrated that coagulation was accelerated (R-time decreased by 0.8±0.4 min (P = 0.001)) and that clot lysis increased (LY60 by 6.0±5.8%-points (P = 0.034)). Plasma coagulation factor VIII and von Willebrand factor ristocetin cofactor activity increased (P = 0.011 and P = 0.024, respectively), demonstrating increased coagulation activity, while von Willebrand factor antigen was unchanged. Plasma protein C activity and tissue-type plasminogen activator increased (P = 0.007 and P = 0.017, respectively), and D-dimer increased by 0.03±0.02 mg l−1 (P = 0.031), demonstrating increased fibrinolytic activity. Plasma prothrombin time and activated partial thromboplastin time were unchanged. Platelet count increased by 15±13% (P = 0.014) and red blood cells by 9±4% (P = 0.002). In humans, LBNP-induced presyncope activates platelets, as evidenced by increased exposure of active glycoprotein IIb/IIIa, accelerates coagulation. LBNP activates fibrinolysis, similar to hemorrhage, but does not alter coagulation screening tests, such as prothrombin time and activated partial thromboplastin time. LBNP results in increased platelet counts, but also in hemoconcentration.

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Section: Discussionmentioning

confidence: 99%

Platelet Activation after Presyncope by Lower Body Negative Pressure in Humans

et al. 2014

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“…V1AR has been shown to be involved in many cellular processes including vascular contraction as well as in the metabolism of glucose, lipids, and protein [38]. Additionally, studies using V1AR knockout mice and isolated cells showed that the V1AR regulates glucose homeostasis [39], mediates the release of aldosterone from adrenal gland cells [38, 40], controls social interactions [41], and platelet aggregation [42, 43]. V1BR mediates the release of adrenocorticotropic hormone and insulin from the pituitary gland and islet cells of the pancreas, respectively [38, 44].…”

Section: Physiologic and Cellular Consequences Of Avp Receptor Sigmentioning

confidence: 99%

Arginine vasopressin receptor signaling and functional outcomes in heart failure

Wasilewski

Myers

Recchia

et al. 2016

Cellular Signalling

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Heart failure (HF) continues to be a highly prevalent syndrome, affecting millions of patients and costing billions of dollars in treatment per year in the United States alone. Studies in failing human heart and in transgenic HF models led to the recognition that enhanced neurohormonal signaling plays a causative role in HF progression, and the use of neurohormone receptor antagonists have proven to decrease hospitalization rates. It has also been long recognized that patients with HF have abnormal water retention, hypo-osmolality, and hyponatremia secondary to elevations in the levels of the neurohormone arginine vasopressin (AVP). AVP is released from the hypothalamus in response to changes in plasma osmolality and pressure, acting at three distinct G protein-coupled receptors: V1AR, V1BR and V2R. Persistent AVP release causes hyponatremia via renal V2R activation, a risk factor for death and hospitalization, and there is a correlation between plasma AVP levels and HF severity/survival of chronic HF patients. Because of the adverse clinical consequences associated with the development of hyponatremia, V2R antagonists were developed for the treatment of HF patients with hyponatremia, however in contrast to other neurohormone blockers they do not relay a survival benefit and may exacerbate decompensated HF requiring inotropic support. Renewed interest in the cardiac V1AR system during HF has arisen due to several recent findings: 1) mice with myocyte-selective transgenic overexpression of cardiac V1AR developed cardiomyopathy in the absence of any pathological insult, 2) cardiac V1AR expression was shown to be increased late-stage human HF, and 3) V1AR antagonism prevented cardiomyopathy development in a mouse model of HF. While cardiac V1AR expression is increased in HF, the role of V1AR signaling in various forms of cardiac injury and in distinct cardiac cell types has been controversial. Therefore this review will primarily focus on V1AR signaling as a potential therapeutic target for HF treatment.

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“…Both ions (sodium and calcium) have been recognized as crucial factors during platelet swelling, ballooning (forming of a balloon-shaped morphology of particularly strongly procoagulant platelets), and PS exposure in platelets adhered to collagen [ 42 ]. NHE plays a pivotal role in controlling platelet swelling—a phenomenon correlating with platelet ballooning and PS exposure [ 29 , 42 , 56 , 57 , 59 , 60 ]—by generation of an osmotic gradient, driving water molecules into platelet cytosol via aquaporins (AQPs). Previously, we reported enhanced ballooning of platelets adhered to collagen after preincubation with adrenaline [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Study on the Mechanism of the Adrenaline-Evoked Procoagulant Response in Human Platelets

Gołaszewska,

Misztal,

Kazberuk

et al. 2024

IJMS

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Adrenaline has recently been found to trigger phosphatidylserine (PS) exposure on blood platelets, resulting in amplification of the coagulation process, but the mechanism is only fragmentarily established. Using a panel of platelet receptors’ antagonists and modulators of signaling pathways, we evaluated the importance of these in adrenaline-evoked PS exposure by flow cytometry. Calcium and sodium ion influx into platelet cytosol, after adrenaline treatment, was examined by fluorimetric measurements. We found a strong reduction in PS exposure after blocking of sodium and calcium ion influx via Na+/H+ exchanger (NHE) and Na+/Ca2+ exchanger (NCX), respectively. ADP receptor antagonists produced a moderate inhibitory effect. Substantial limitation of PS exposure was observed in the presence of GPIIb/IIIa antagonist, phosphoinositide-3 kinase (PI3-K) inhibitors, or prostaglandin E1, a cyclic adenosine monophosphate (cAMP)-elevating agent. We demonstrated that adrenaline may develop a procoagulant response in human platelets with the substantial role of ion exchangers (NHE and NCX), secreted ADP, GPIIb/IIIa-dependent outside-in signaling, and PI3-K. Inhibition of the above mechanisms and increasing cytosolic cAMP seem to be the most efficient procedures to control adrenaline-evoked PS exposure in human platelets.

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Vasopressin acts on platelets to generate procoagulant activity

Cited by 17 publications

References 38 publications

Platelet Activation after Presyncope by Lower Body Negative Pressure in Humans

Platelet Activation after Presyncope by Lower Body Negative Pressure in Humans

Arginine vasopressin receptor signaling and functional outcomes in heart failure

Study on the Mechanism of the Adrenaline-Evoked Procoagulant Response in Human Platelets

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