Abstract 025: AMP-activated Protein Kinase Mediates Pressure Overload-induced Hypertrophy

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Jinli Wang ◽  
Nanhu Quan ◽  
Lin Wang ◽  
Courtney Cates ◽  
Ji Li
Keyword(s):  
Blood Pressure ◽  
Protein Kinase ◽  
High Blood Pressure ◽  
Morphological Changes ◽  
Heart Function ◽  
Pressure Overload ◽  
Vascular Diseases ◽  
Adenosine Monophosphate ◽  
Macrophage Infiltration ◽  
Therapeutic Drug

Hypertension is a major risk factor of death and disability from heart and vascular diseases. Heart hypertrophy caused by pressure overload is characterized by the activation of adenosine monophosphate-activated protein kinase (AMPK), which is the major energy sensor in the heart. However, the anti-inflammatory effect of AMPK has not been investigated in the hypertrophy model. Activated protein C (APC) is a vitamin-K dependent plasma serine protease which inhibits blood clotting, and APC is an endogenous AMPK agonist. This study was designed to examine the role of AMPK in hypertrophy and the underlying mechanisms by which APC inhibits heart hypotrophy by pressure overload. We hypothesize that AMPK play a role in preventing heart from hypertrophy induced by pressure overload. APC could inhibit high blood pressure-induced hypertrophy via activation of AMPK signaling pathway. Wild-type (WT) and AMPK-kinase dead (KD) transgenic mice were subjected to transverse aortic constriction (TAC) surgery. Echocardiography was performed to evaluate the heart function, and histology staining revealed the morphological changes. Real-time PCR and western blotting were used to detect the signaling changes of both mRNA and protein expression levels. There is no phenotype difference between WT and AMPK-KD mice under normal physiological conditions. However after 4 weeks of TAC surgery, AMPK-KD mice demonstrated significantly bigger heart than WT mice (p<0.05), and the cardiac functions measured by echocardiography in AMPK-KD hearts were significantly impaired as compared with WT hearts (p<0.05). The immunohistochemical staining showed that the increased macrophage infiltration and reactive oxygen species (ROS) including activated p66shc, 4-HNE and ERK were observed in the AMPK-KD hearts after 4 weeks of TAC surgery (all p<0.05 versus WT hearts). APC administration significantly attenuated hypertrophy and fibrosis caused by pressure overload, and macrophage infiltration and p66shc activation were also inhibited by APC treatment. Therefore, Cardiac AMPK deficiency aggravates hypertrophy caused by pressure overload. AMPK activator APC could be a therapeutic drug for treatment of hypertrophy by high blood pressure.

Abstract 319: Cardiac Deficiency of AMPK Exacerbates Heart Hypertrophy by Pressure Overload

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Jinli Wang ◽  
Nanhu Quan ◽  
Lin Wang ◽  
Wanqing Sun ◽  
Courtney A Cates ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Morphological Changes ◽  
Heart Function ◽  
Activated Protein C ◽  
Pressure Overload ◽  
Adenosine Monophosphate ◽  
Macrophage Infiltration ◽  
Therapeutic Drug ◽  
Heart Hypertrophy

Introduction: Heart hypertrophy caused by pressure overload is characterized by the activation of adenosine monophosphate-activated protein kinase (AMPK), which is a major energy sensor in the heart. However, the anti-inflammatory effect of AMPK has not been determined in the hypertrophy model. Activated protein C (APC) is a vitamin-K dependent plasma serine protease which inhibits blood clotting, and APC is an endogenous AMPK agonist. This study was designed to examine the role of AMPK in hypertrophy and the underlying mechanisms by which APC inhibits heart hypotrophy by pressure overload. Hypothesis: AMPK play a role in preventing heart from hypertrophy induced by pressure overload. APC could inhibit high blood pressure-induced hypertrophy via activation of AMPK signaling pathway. Methods: Wild-type (WT) and AMPK-kinase dead (KD) transgenic mice were subjected to transverse aortic constriction (TAC) surgery. Echocardiography was performed to evaluate the heart function, and histology staining revealed the morphological changes. Real-time PCR and western blotting were used to determine the signaling changes of mRNA and protein expression levels. Results: There is no phenotype difference between WT and AMPK-KD mice under normal physiological conditions. However after 4 weeks of TAC surgery, AMPK-KD mice demonstrated significantly bigger heart than WT mice (p<0.05), and the cardiac functions measured by echocardiography in AMPK-KD hearts were significantly impaired as compared with WT hearts (p<0.05). The immunohistochemical staining showed that the increased macrophage infiltration and reactive oxygen species (ROS) including activated p66shc, 4-Hydroxynonenal accumulation and phosphorylation of extracellular signal-regulated kinase (ERK) were observed in the AMPK-KD hearts after 4 weeks of TAC surgery (all p<0.05 versus WT hearts). APC administration significantly attenuated hypertrophy and fibrosis caused by pressure overload, and macrophage infiltration and p66shc activation were also inhibited by APC treatment. Conclusions: Cardiac AMPK deficiency aggravates hypertrophy caused by pressure overload. AMPK activator APC could be a therapeutic drug for treatment of hypertrophy by high blood pressure.

The Effect of Green Coffee Consumption on High Blood Pressure

2021 ◽  
Author(s):  
Mahdieh Hosseinzadeh ◽  
Fatemeh Pakravanfar ◽  
Elham Hosseinzadeh ◽  
Maryam Khosravi
Keyword(s):  
Blood Pressure ◽  
Clinical Trials ◽  
High Blood Pressure ◽  
Coffee Consumption ◽  
Vascular Diseases ◽  
Publication Date ◽  
Green Coffee ◽  
Chlorogenic Acids ◽  
Coffee Intake ◽  
Randomized Controlled Clinical Trials

Background: Hypertension is a major risk factor for the development of coronary, cerebrovascular, and peripheral vascular diseases, which lead to myocardial infarction, stroke, and vascular death. Green coffee extract is particularly producer a great deal of chlorogenic acids (CGA) that may reduce the risk of high blood pressure. Therefore, the target of the study was to summarize the available publications on the effect of green coffee consumption on high blood pressure. Methods: The systematic review was done with a search in PubMed-Medline and Scopus. The search strategy included keywords related to blood pressure and green coffee. Inclusion criteria were randomized controlled clinical trials conducted on people aged between 18 and 70 years. The publication date of articles  was from 2004 to 2018. Exclusion criteria were articles not published in English. Results: We discussed five articles that included  our criteria. Green coffee had moderate effects on high blood pressure.  It sounds that the effect of green coffee on reducing blood pressure is because of its phenolic compounds, as well as caffeine and chlorogenic acids, coffee’s roasting status, participants’ ethnicity, and even gender. Conclusion: Green coffee intake for a long time might moderately decrease blood pressure. However, there is still a need for further clinical trials.

scholarly journals Life style habits of truck drivers in France

2019 ◽  
Vol 29 (Supplement_4) ◽  
Author(s):  
V Bourdin ◽  
G King ◽  
L Josseran
Keyword(s):  
Blood Pressure ◽  
Alcohol Consumption ◽  
High Blood Pressure ◽  
Vascular Diseases ◽  
Daily Basis ◽  
Cross Sectional Study ◽  
Truck Drivers ◽  
Road Accidents ◽  
Cross Sectional ◽  
Significant Difference

Abstract Background European truck drivers’ (TD) lifestyle behaviors is a topic of great interest but not frequently studied. Unhealthy behaviors such as smoking, alcohol consumption, drug abuse or a lack of physical activity infer a greater risk for cardio-vascular diseases and road accidents. This study aimed at describing life TD habits. Methods A prospective cross-sectional study was conducted in April 2018 on 4 rest areas with the support of the nonprofit organization “Fondation VINCI Autoroutes pour une Conduite Responsable”. 515 TD were interviewed randomly at 4 highway rest stops. Life habits data were collected and analysis was conducted using univariate statistics. Results 38.6% (n = 199) declared to be daily smokers, with no significant difference when reported to nationality or age. 24.6% (n = 126) are normal weighted, while 72.4% (n = 373) have a BMI superior to 25. 58.8% (n = 303) of the TD drink alcohol on a regular basis, and 8.5% of them (n = 26) on a daily basis. High blood pressure is significatively associated with alcohol consumption (5.2% vs. 12.9%, p &lt; 0,05) and obesity (19.4 % vs. &lt; 10%, p &lt; 0,001). 2.5% (n = 13) of the TD consume psychoactive drugs, most of them cannabis. As concerns diet: 32.8% (n = 169) consider it as balanced, 32.6% (n = 168) not balanced, and 34,6% can’t qualify it. When TD think their diet is unbalanced, they judge it too fat (75.6%), too sweet (61.9%) or too salty (50.6%). Conclusions The most striking results concern TD expectations, since 41.7% of the daily smokers and 5.3% of the alcohol consumers would be interested in help measures to stop. TD with the highest BMI are the most demanding for a diet help. Motorway operators, unions and compagnies should fulfill these expectations, since TD in better health are less frequently involve in road accidents. TD spend a lot of time on rest area and this offers interesting periods of time to develop health education specifically for them. Key messages Many truck drivers prove to be daily smokers and/or with excess weight, and/or eating an unbalanced diet. High blood pressure is significatively associated with alcohol consumption and obesity. Expectations are high as concerns help measures to reach healthier behaviors and live a better life.

scholarly journals Direct Cardiac Actions of the Sodium Glucose Co‐Transporter 2 Inhibitor Empagliflozin Improve Myocardial Oxidative Phosphorylation and Attenuate Pressure‐Overload Heart Failure

2021 ◽  
Author(s):  
Xuan Li ◽  
Qingguo Lu ◽  
Yunguang Qiu ◽  
Jussara M. do Carmo ◽  
Zhen Wang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protein Kinase ◽  
Oxidative Phosphorylation ◽  
Mammalian Target Of Rapamycin ◽  
Pressure Overload ◽  
Adenosine Monophosphate ◽  
Transverse Aortic Constriction ◽  
Diabetic Mellitus ◽  
Aortic Constriction ◽  
Cardiac Effects

Background We determined if the sodium glucose co‐transporter 2 inhibitor empagliflozin attenuates pressure overload‐induced heart failure in non‐diabetic mellitus mice by direct cardiac effects and the mechanisms involved. Methods and Results Male C57BL/6J mice (4–6 months of age) were subjected to sham surgeries or transverse aortic constriction to produce cardiac pressure overload. Two weeks after transverse aortic constriction, empagliflozin (10 mg/kg per day) or vehicle was administered daily for 4 weeks. Empagliflozin increased survival rate and significantly attenuated adverse left ventricle remodeling and cardiac fibrosis after transverse aortic constriction. Empagliflozin also attenuated left ventricular systolic and diastolic dysfunction, evaluated by echocardiography, and increased exercise endurance by 36% in mice with transverse aortic constriction‐induced heart failure. Empagliflozin significantly increased glucose and fatty acid oxidation in failing hearts, while reducing glycolysis. These beneficial cardiac effects of empagliflozin occurred despite no significant changes in fasting blood glucose, body weight, or daily urine volume. In vitro experiments in isolated cardiomyocytes indicated that empagliflozin had direct effects to improve cardiomyocyte contractility and calcium transients. Importantly, molecular docking analysis and isolated perfused heart experiments indicated that empagliflozin can bind cardiac glucose transporters to reduce glycolysis, restore activation of adenosine monophosphate‐activated protein kinase and inhibit activation of the mammalian target of rapamycin complex 1 pathway. Conclusions Our study demonstrates that empagliflozin may directly bind glucose transporters to reduce glycolysis, rebalance coupling between glycolysis and oxidative phosphorylation, and regulate the adenosine monophosphate‐activated protein kinase mammalian target of rapamycin complex 1 pathway to attenuate adverse cardiac remodeling and progression of heart failure induced by pressure‐overload in non‐diabetic mellitus mice.

scholarly journals Increased Adenosine Monophosphate–Activated Protein Kinase Activity in Rat Hearts With Pressure-Overload Hypertrophy

Circulation ◽  
2001 ◽  
Vol 104 (14) ◽  
pp. 1664-1669 ◽  
Author(s):  
Rong Tian ◽  
Nicolas Musi ◽  
Jessica D’Agostino ◽  
Michael F. Hirshman ◽  
Laurie J. Goodyear
Keyword(s):  
Protein Kinase ◽  
Kinase Activity ◽  
Pressure Overload ◽  
Adenosine Monophosphate ◽  
Protein Kinase Activity ◽  
Rat Hearts

Buckling Behavior of Arteries Under Torsion

2011 ◽  
Author(s):  
Justin R. Garcia ◽  
Shawn D. Lamm ◽  
Hai-Chao Han
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Blood Vessels ◽  
High Blood Pressure ◽  
Atherosclerotic Plaque ◽  
Vascular Grafts ◽  
Vascular Diseases ◽  
The Body ◽  
Buckling Behavior ◽  
Surgical Implantation

Arterial tortuosity is a phenomenon which is observed throughout the body and is associated with aging, diabetes, high blood pressure, and other vascular diseases [1]. Tortuous arteries significantly hinder blood flow which may lead to the development of atherosclerotic plaque buildup [2]. Blood vessels may also become twisted or demonstrate 3-D tortuous shapes when subject to large twist deformations such as during surgical implantation of vascular grafts, propeller flap procedures, stent-artery interactions, and sudden movements of the neck or limbs [4–6]. However, the twisting behavior of arteries is poorly understood.

Long-term activation of adenosine monophosphate-activated protein kinase attenuates pressure-overload-induced cardiac hypertrophy

2007 ◽  
Vol 100 (5) ◽  
pp. 1086-1099 ◽  
Author(s):  
Hong-Liang Li ◽  
Ran Yin ◽  
Dandan Chen ◽  
Dan Liu ◽  
Dong Wang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cardiac Hypertrophy ◽  
Pressure Overload ◽  
Adenosine Monophosphate
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