scholarly journals 'Role reversal' for the receptor PAR1 in sepsis-induced vascular damage

2007 ◽  
Vol 8 (12) ◽  
pp. 1303-1312 ◽  
Author(s):  
Nicole C Kaneider ◽  
Andrew J Leger ◽  
Anika Agarwal ◽  
Nga Nguyen ◽  
George Perides ◽  
...  
Keyword(s):  
Role Reversal ◽  
Vascular Damage

Using role reversal

2011 ◽  
Author(s):  
Peter L. Kranz
Keyword(s):  
Role Reversal

Targeting the Endothelial Ca2+ Toolkit to Rescue Endothelial Dysfunction in Obesity Associated-Hypertension

2020 ◽  
Vol 27 (2) ◽  
pp. 240-257 ◽  
Author(s):  
Francesco Moccia ◽  
Sharon Negri ◽  
Pawan Faris ◽  
Roberto Berra-Romani
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Endothelial Damage ◽  
Vascular Damage ◽  
Zucker Rats ◽  
Bibliographic Databases ◽  
Resistance Arteries ◽  
Small Resistance ◽  
Obese Zucker Rats ◽  
Transient Receptor

Background: Obesity is a major cardiovascular risk factor which dramatically impairs endothelium- dependent vasodilation and leads to hypertension and vascular damage. The impairment of the vasomotor response to extracellular autacoids, e.g., acetylcholine, mainly depends on the reduced Nitric Oxide (NO) bioavailability, which hampers vasorelaxation in large conduit arteries. In addition, obesity may affect Endothelium-Dependent Hyperpolarization (EDH), which drives vasorelaxation in small resistance arteries and arterioles. Of note, endothelial Ca2+ signals drive NO release and trigger EDH. Methods: A structured search of bibliographic databases was carried out to retrieve the most influential, recent articles on the impairment of vasorelaxation in animal models of obesity, including obese Zucker rats, and on the remodeling of the endothelial Ca2+ toolkit under conditions that mimic obesity. Furthermore, we searched for articles discussing how dietary manipulation could be exploited to rescue Ca2+-dependent vasodilation. Results: We found evidence that the endothelial Ca2+ could be severely affected by obese vessels. This rearrangement could contribute to endothelial damage and is likely to be involved in the disruption of vasorelaxant mechanisms. However, several Ca2+-permeable channels, including Vanilloid Transient Receptor Potential (TRPV) 1, 3 and 4 could be stimulated by several food components to stimulate vasorelaxation in obese individuals. Conclusion: The endothelial Ca2+ toolkit could be targeted to reduce vascular damage and rescue endothelium- dependent vasodilation in obese vessels. This hypothesis remains, however, to be probed on truly obese endothelial cells.

Immune System Alterations by Aldosterone During Hypertension: From Clinical Observations to Genomic and Non-Genomic Mechanisms Leading to Vascular Damage

2013 ◽  
Vol 13 (6) ◽  
pp. 1035-1046 ◽  
Author(s):  
N. Munoz-Durango ◽  
M.F. Barake ◽  
N.A. Letelier ◽  
C. Campino ◽  
C.E. Fardella ◽  
...  
Keyword(s):  
Immune System ◽  
Vascular Damage ◽  
Clinical Observations

Sympathetic drive and vascular damage in hypertension and atherosclerosis.

Hypertension ◽  
1991 ◽  
Vol 17 (4_Suppl) ◽  
pp. III75-III75 ◽  
Author(s):  
P. Pauletto ◽  
G. Scannapieco ◽  
A. C. Pessina
Keyword(s):  
Vascular Damage

scholarly journals Colonization of dermal arterioles by Neisseria meningitidis provides a safe haven from neutrophils

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Valeria Manriquez ◽  
Pierre Nivoit ◽  
Tomas Urbina ◽  
Hebert Echenique-Rivera ◽  
Keira Melican ◽  
...  
Keyword(s):  
Neisseria Meningitidis ◽  
Inflammatory Infiltrate ◽  
Immune Escape ◽  
Systemic Disease ◽  
Neutrophil Recruitment ◽  
Vascular Damage ◽  
Bacterial Burden ◽  
Human Pathogen ◽  
Humanized Mouse ◽  
Humanized Mouse Model

AbstractThe human pathogen Neisseria meningitidis can cause meningitis and fatal systemic disease. The bacteria colonize blood vessels and rapidly cause vascular damage, despite a neutrophil-rich inflammatory infiltrate. Here, we use a humanized mouse model to show that vascular colonization leads to the recruitment of neutrophils, which partially reduce bacterial burden and vascular damage. This partial effect is due to the ability of bacteria to colonize capillaries, venules and arterioles, as observed in human samples. In venules, potent neutrophil recruitment allows efficient bacterial phagocytosis. In contrast, in infected capillaries and arterioles, adhesion molecules such as E-Selectin are not expressed on the endothelium, and intravascular neutrophil recruitment is minimal. Our results indicate that the colonization of capillaries and arterioles by N. meningitidis creates an intravascular niche that precludes the action of neutrophils, resulting in immune escape and progression of the infection.

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