Endothelial Dysfunction in Chronic Myocardial Infarction Despite Increased Vascular Endothelial Nitric Oxide Synthase and Soluble Guanylate Cyclase Expression

Although the endothelial dysfunction is related with tumor development, there is no consensus on the suppressive or supportive effect on tumor growth. The goal of the present study was to evaluate endothelial dysfunction related factors in animal breast cancer model that was developed by administrating endothelial nitric oxide synthase blocking agent, Nitro-L-arginine methyl ester hydrochloride (L-NAME). Endothelial dysfunction related main factors such as nitric oxide synthase, interleukin-6, vascular endothelial growth factor receptor-2 and vascular endothelial cadherin were investigated by immunohistochemically in tumor and carotid artery tissues. In tumor tissues apoptosis was determined by TUNEL assay. The level of endothelin-1 in blood was measured by ELISA. İntima-media thickness of carotid artery was evaluated with Doppler-USG measurements. As a result, in this study it was shown that vascular endothelial growth factor receptor-2, endothelin-1, endothelial nitric oxide synthase, interleukin-6, vascular endothelial cadherin and E-selectin molecules play a role in reducing breast tumor growth based on endothelial dysfunction.

Download Full-text

Changes of soluble CD40 ligand in the progression of acute myocardial infarction associate to endothelial nitric oxide synthase polymorphisms and vascular endothelial growth factor but not to platelet CD62P expression

Translational Research ◽

10.1016/j.trsl.2015.07.006 ◽

2015 ◽

Vol 166 (6) ◽

pp. 650-659 ◽

Cited By ~ 11

Author(s):

Patrícia Napoleão ◽

Maria do Céu Monteiro ◽

Luís B.P. Cabral ◽

Maria Begoña Criado ◽

Catarina Ramos ◽

...

Keyword(s):

Nitric Oxide ◽

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Endothelial Nitric Oxide Synthase ◽

Cd40 Ligand ◽

Vascular Endothelial ◽

Soluble Cd40 Ligand ◽

Oxide Synthase ◽

Endothelial Growth Factor ◽

Endothelial Nitric Oxide

Download Full-text

Vascular endothelial dysfunction with aging: endothelin-1 and endothelial nitric oxide synthase

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00689.2008 ◽

2009 ◽

Vol 297 (1) ◽

pp. H425-H432 ◽

Cited By ~ 173

Author(s):

Anthony J. Donato ◽

Lindsey B. Gano ◽

Iratxe Eskurza ◽

Annemarie E. Silver ◽

Phillip E. Gates ◽

...

Keyword(s):

Nitric Oxide ◽

Endothelial Dysfunction ◽

Brachial Artery ◽

Endothelial Nitric Oxide Synthase ◽

Older Men ◽

Vascular Endothelial ◽

Vascular Endothelial Dysfunction ◽

Healthy Men ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

To determine whether impaired endothelium-dependent dilation (EDD) in older adults is associated with changes in the expression of major vasoconstrictor or vasodilator proteins in the vascular endothelium, endothelial cells (EC) were obtained from the brachial artery and peripheral veins of 56 healthy men, aged 18–78 yr. Brachial artery EC endothelin-1 (ET-1) [0.99 ± 0.10 vs. 0.57 ± 0.10 ET-1/human umbilical vein EC (HUVEC) intensity, P = 0.01] and serine 1177 phosphorylated endothelial nitric oxide synthase (PeNOS) (0.77 ± 0.09 vs. 0.44 ± 0.07 PeNOS/HUVEC intensity, P < 0.05) (quantitative immunofluorescence) were greater, and EDD (peak forearm blood flow to intrabrachial acetylcholine) was lower (10.2 ± 0.9 vs. 14.7 ± 1.7 ml·100 ml−1·min−1, P < 0.05) in older ( n = 18, 62 ± 1 yr) vs. young ( n = 15, 21 ± 1 yr) healthy men. EDD was inversely related to expression of ET-1 ( r = −0.39, P < 0.05). Brachial artery EC eNOS expression did not differ significantly with age, but tended to be greater in the older men (young: 0.23 ± 0.03 vs. older: 0.33 ± 0.07 eNOS/HUVEC intensity, P = 0.08). In the sample with venous EC collections, EDD (brachial artery flow-mediated dilation) was lower (3.50 ± 0.44 vs. 7.68 ± 0.43%, P < 0.001), EC ET-1 and PeNOS were greater ( P < 0.05), and EC eNOS was not different in older ( n = 23, 62 ± 1 yr) vs. young ( n = 27, 22 ± 1 yr) men. EDD was inversely related to venous EC ET-1 ( r = −0.37, P < 0.05). ET-1 receptor A inhibition with BQ-123 restored 60% of the age-related impairment in carotid artery dilation to acetylcholine in B6D2F1 mice (5–7 mo, n = 8; 30 mo, n = 11; P < 0.05). ET-1 expression is increased in vascular EC of healthy older men and is related to reduced EDD, whereas ET-1 receptor A signaling tonically suppresses EDD in old mice. Neither eNOS nor PeNOS is reduced with aging. Changes in ET-1 expression and bioactivity, but not eNOS, contribute to vascular endothelial dysfunction with aging.

Download Full-text