Research LettersImpaired capacity for endogenous fibrinolysis in essential hypertension
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Cited by (62)
Valproic acid selectively increases vascular endothelial tissue-type plasminogen activator production and reduces thrombus formation in the mouse
2016, Journal of Thrombosis and HaemostasisD-dimer relates positively with increased blood pressure in black South Africans: The SABPA study
2014, Thrombosis ResearchCitation Excerpt :t-PA is responsible for the activation of plasminogen into plasmin that results in the lysis of fibrin into fibrin degradation products and is released from the endothelial cells at a steady rate [44]. However, changes in blood constituents and flow as well as endothelial dysfunction may result in an increased release of t-PA and PAI-1 from the endothelial cells [15,45,46]. During conditions such as uncontrolled hypertension, t-PA release from the intracellular storage pools may be depleted and subsequently PAI-1 secretion may overtake t-PA production, impairing the fibrinolytic pathway that results in a longer CLT as well as the formation of a fibrin clot that is more resilient to lysis [47–49].
Systemic circulation
2010, Paediatric CardiologyTranscutaneous electrical nerve stimulation induces vasodilation in healthy controls but not in refractory angina patients
2010, Journal of Pain and Symptom ManagementCitation Excerpt :It has been suggested that these effects may be secondary to an induced myocardial release of β-endorphin by means of an agonistic effect on local mu-receptors.15 Other mechanisms, such as inhibition of sympathetic activity, also have been proposed.16–18 Although this suggests that the vascular response of TENS might differ between patients with atherosclerotic disease and healthy subjects, these studies have been performed in completely different vascular beds.
Systemic Circulation
2009, Paediatric CardiologyInfluence of TNF-α and biomechanical stress on endothelial anti- and prothrombotic genes
2009, Biochemical and Biophysical Research CommunicationsCitation Excerpt :To our surprise, anti- and prothrombotic genes in ECs seemed to be insensitive to tensile stress. We have previously shown that essential hypertension, which we thought mainly induced an increased tensile stress, was associated with a defective t-PA release capacity in vivo[15,16]. Previous studies have shown that genes non-responsive to TNF-α were shifted to a TNF-α sensitive state by biomechanical stress [17].