scholarly journals Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk

Nature ◽  
2011 ◽  
Vol 478 (7367) ◽  
pp. 103-109 ◽  
Author(s):  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Genetic Variants ◽  
Disease Risk ◽  
Cardiovascular Disease Risk

scholarly journals Age modification of ozone associations with cardiovascular disease risk in adults: a potential role for soluble P-selectin and blood pressure

2018 ◽  
Vol 10 (7) ◽  
pp. 4643-4652 ◽  
Author(s):  
Drew B. Day ◽  
Merlise A. Clyde ◽  
Jianbang Xiang ◽  
Feng Li ◽  
Xiaoxing Cui ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Potential Role ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Soluble P

scholarly journals Vitamin D Receptor Activation Mitigates the Impact of Uremia on Endothelial Function in the 5/6 Nephrectomized Rats

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
J. Ruth Wu-Wong ◽  
William Noonan ◽  
Masaki Nakane ◽  
Kristin A. Brooks ◽  
Jason A. Segreti ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Heart Rate ◽  
Vitamin D ◽  
Endothelial Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Receptor Activation ◽  
The Impact

Endothelial dysfunction increases cardiovascular disease risk in chronic kidney disease (CKD). This study investigates whether VDR activation affects endothelial function in CKD. The 5/6 nephrectomized (NX) rats with experimental chronic renal insufficiency were treated with or without paricalcitol, a VDR activator. Thoracic aortic rings were precontracted with phenylephrine and then treated with acetylcholine or sodium nitroprusside. Uremia significantly affected aortic relaxation (% in NX rats versus % in SHAM at 30 M acetylcholine). The endothelial-dependent relaxation was improved to –%, –%, and –% in NX rats treated with paricalcitol at 0.021, 0.042, and 0.083 g/kg for two weeks, respectively, while paricalcitol at 0.042 g/kg did not affect blood pressure and heart rate. Parathyroid hormone (PTH) suppression alone did not improve endothelial function since cinacalcet suppressed PTH without affecting endothelial-dependent vasorelaxation. N-omega-nitro-L-arginine methyl ester completely abolished the effect of paricalcitol on improving endothelial function. These results demonstrate that VDR activation improves endothelial function in CKD.

scholarly journals Left Ventricular Mass Index Is Associated With Cognitive Function in Middle-Age

2020 ◽  
Vol 13 (8) ◽  
Author(s):  
Alexander C. Razavi, ◽  
Camilo Fernandez ◽  
Jiang He ◽  
Tanika N. Kelly ◽  
Marie Krousel-Wood ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Cognitive Function ◽  
Systolic Blood Pressure ◽  
Middle Age ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Left Ventricular ◽  
Lv Mass ◽  
Lv Remodeling

Background: Elevated cardiovascular disease risk factor burden is a recognized contributor to poorer cognitive function; however, the physiological mechanisms underlying this association are not well understood. We sought to assess the potential mediation effect of left ventricular (LV) remodeling on the association between lifetime systolic blood pressure and cognitive function in a community-based cohort of middle-aged adults. Methods: Nine hundred sixty participants of the Bogalusa Heart Study (59.2% women, 33.8% black, aged 48.4±5.1 years) received 2-dimensional echocardiography to quantify relative wall thickness, LV mass, and diastolic and systolic LV function; and a standardized neurocognitive battery to assess memory, executive functioning, and language processing. Multivariable linear regression assessed the association of cardiac structure and function with a global composite cognitive function score, adjusting for traditional cardiovascular disease risk factors. Mediation analysis assessed the effect of LV mass index on the association between lifetime systolic blood pressure burden and cognitive function. Results: There were 233 (24.3%) and 136 (14.2%) individuals with concentric LV remodeling and concentric LV hypertrophy, respectively. Each g/m 2.7 increment in LV mass index was associated with a 0.03 standardized unit decrement in global cognitive function ( P =0.03). Individuals with concentric LV remodeling and isolated diastolic dysfunction had the poorest cognitive function, and a greater ratio between early mitral inflow velocity and early diastolic mitral annular velocity (E/e’) was associated with poorer cognitive function, even after adjustment for LV mass index (B=−0.12; P =0.03). A total of 18.8% of the association between lifetime systolic blood pressure burden and midlife cognitive function was accounted for by LV mass index. Conclusions: Cardiac remodeling partially mediates the association between lifespan systolic blood pressure burden and adult cognition in individuals without dementia or clinical cardiovascular disease. Slowing or reversing the progression of cardiac remodeling in middle-age may be a novel therapeutic approach to prevent cognitive decline.

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