Effects of Calcium Antagonistic and Agonistic Dihydropyridines on Experimental Hypertension and Vascular Damage

1985 ◽  
pp. 412-422
Author(s):  
S. Kazda ◽  
B. Garthoff ◽  
G. Luckhaus
Keyword(s):  
Vascular Damage ◽  
Experimental Hypertension

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 Resveratrol Protects Cardiac Tissue in Experimental Malignant Hypertension Due to Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Properties

2021 ◽  
Vol 22 (9) ◽  
pp. 5006
Author(s):  
Jelica Grujić-Milanović ◽  
Vesna Jaćević ◽  
Zoran Miloradović ◽  
Djurdjica Jovović ◽  
Ivica Milosavljević ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Diseases ◽  
Cardiac Tissue ◽  
Morphological Changes ◽  
Chronic Administration ◽  
Heart Tissue ◽  
Severe Form ◽  
Malignant Hypertension ◽  
Experimental Hypertension ◽  
Resveratrol Treatment

Hypertension is one of the most prevalent and powerful contributors of cardiovascular diseases. Malignant hypertension is a relatively rare but extremely severe form of hypertension accompanied with heart, brain, and renal impairment. Resveratrol, a recently described grape-derived, polyphenolic antioxidant molecule, has been proposed as an effective agent in the prevention of cardiovascular diseases. This study was designed to examine chronic resveratrol administration on blood pressure, oxidative stress, and inflammation, with special emphasis on cardiac structure and function in two models of experimental hypertension. The experiments were performed in spontaneously (SHRs) and malignantly hypertensive rats (MHRs). The chronic administration of resveratrol significantly decreased blood pressure in both spontaneously and malignant hypertensive animals. The resveratrol treatment ameliorated morphological changes in the heart tissue. The immunohistochemistry of the heart tissue after resveratrol treatment showed that both TGF-β and Bax were not present in the myocytes of SHRs and were present mainly in the myocytes of MHRs. Resveratrol suppressed lipid peroxidation and significantly improved oxidative status and release of NO. These results suggest that resveratrol prevents hypertrophic and apoptotic consequences induced by high blood pressure with more pronounced effects in malignant hypertension.

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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