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Platelet inhibition by hypochlorous acid involves cAMP signalling.
Cell Signal
December 2024
UCD School of Medicine, UCD Conway Institute, University College Dublin, Dublin 4, Belfield, Ireland; Irish Centre for Vascular Biology, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin D02 YN77, Ireland. Electronic address:
Hypochlorous acid (HOCl), made by neutrophil-derived myeloperoxidase, has been suggested to inhibit platelets, however, the mechanisms involved have not been described. Here we confirm that HOCl exposure changes platelet morphology and inhibits platelet spreading and aggregation. HOCl effects could be reversed by glutathione suggesting a role for cysteine oxidation.
View Article and Find Full Text PDFEffects of exercise on cAMP-mediated platelet inhibition in young women: a pilot study.
Eur J Appl Physiol
December 2024
UCD School of Medicine, UCD Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland.
Purpose: Exercise has been shown to reduce platelet reactivity and increase platelet sensitivity to prostacyclin, an endothelium-derived inhibitor of platelet activation, in middle-aged men and women. It is currently unknown if these beneficial effects can also be observed in young women and the intracellular mechanisms involved have not been identified. In this study, the feasibility of detecting changes in platelet reactivity, prostacyclin sensitivity and cAMP signalling were tested.
View Article and Find Full Text PDFEarly vascular aging in chronic kidney disease: focus on microvascular maintenance, senescence signature and potential therapeutics.
Transl Res
January 2025
Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden. Electronic address:
Chronic kidney disease (CKD) is a strong risk factor for cardiovascular mortality and morbidity. We hypothesized that a senescent phenotype instigated by uremic toxins could account for early vascular aging (EVA) and vascular dysfunctions of microvasculature in end stage kidney disease (ESKD) patients which ultimately lead to increased cardiovascular complication. To test this hypothesis, we utilized both in vivo, and ex vivo approaches to study endothelial and smooth muscle function and structure, and characterized markers related to EVA in 82 ESKD patients (eGFR <15 ml/min) and 70 non-CKD controls.
View Article and Find Full Text PDFEndothelial epoxyeicosatrienoic acid release is intact in aldosterone excess.
Atherosclerosis
November 2024
Department of Medicine IV, LMU University Hospital, LMU Munich, Munich, Germany. Electronic address:
Article Synopsis
- Endothelial dysfunction (ED) is linked to higher cardiovascular disease rates in primary aldosteronism (PA), and the role of the epoxyeicosatrienoic acid (EET) pathway in this context is not well-understood.
- The study analyzed how aldosterone impacts EET production and endothelial function by using various methods, including qPCR, calcium imaging, and mass spectrometry on both human cells and patient plasma.
- Findings suggest that while aldosterone alters inflammation and calcium responses in endothelial cells, it does not hinder EET release, indicating that targeting epoxide hydrolase might help reverse these endothelial issues and warrants further investigation as a potential treatment.
Hypertensive Emergency During Dialysis: A Paradoxical Physiologic Response.
Cureus
May 2024
Nephrology, Jersey Shore University Medical Center, Neptune City, USA.
Most end-stage renal disease patients experience a reduction in blood pressure during their hemodialysis session compared to predialysis. Surprisingly, a small subset of patients will experience an unusual physiological response to dialysis that results in a paradoxical increase in blood pressure. We discuss a case that involved an exaggerated elevation in blood pressure, ultimately requiring immediate cessation of dialysis and admission to the intensive care unit for intravenous treatment of a hypertensive emergency.
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