Fatty acids (FAs) are acquired from free FA associated with albumin and lipoprotein triglyceride that is hydrolyzed by lipoprotein lipase (LpL). Hypertrophied hearts shift their substrate usage pattern to more glucose and less FA. However, FAs may still be an important source of energy in hypertrophied hearts. The aim of this study was to examine the importance of LpL-derived FAs in hypertensive hypertrophied hearts. We followed cardiac function and metabolic changes during 2 wk of angiotensin II (ANG II)-induced hypertension in control and heart-specific lipoprotein lipase knockout (hLpL0) mice. Glucose metabolism was increased in ANG II-treated control (control/ANG II) hearts, raising it to the same level as hLpL0 hearts. FA uptake-related genes, CD36 and FATP1, were reduced in control/ANG II hearts to levels found in hLpL0 hearts. ANG II did not alter these metabolic genes in hLpL0 mice. LpL activity was preserved, and mitochondrial FA oxidation-related genes were not altered in control/ANG II hearts. In control/ANG II hearts, triglyceride stores were consumed and reached the same levels as in hLpL0/ANG II hearts. Intracellular ATP content was reduced only in hLpL0/ANG II hearts. Both ANG II and deoxycorticosterone acetate-salt induced hypertension caused heart failure only in hLpL0 mice. Our data suggest that LpL activity is required for normal cardiac metabolic compensation to hypertensive stress.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2536729 | PMC |
| http://dx.doi.org/10.1152/ajpendo.90338.2008 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Background Menopause is associated with an increase in the prevalence and severity of hypertension in women. Although premenopausal females are protected against T cell-dependent immune activation and development of angiotensin II (Ang II) hypertension, this protection is lost in postmenopausal females. Therefore, the current study hypothesized that specific CD4 T cell pathways are regulated by sex hormones and Ang II to mediate progression from premenopausal protection to postmenopausal hypertension.
View Article and Find Full Text PDFAngiotensin II and salt-induced decompensation in Balb/CJ mice is aggravated by fluid retention related to low oxidative stress.
Am J Physiol Renal Physiol
May 2019
Integrative Physiology, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Balb/CJ mice are more sensitive to treatment with angiotensin II (ANG II) and high-salt diet compared with C57BL/6J mice. Together with higher mortality, they develop edema, signs of heart failure, and acute kidney injury. The aim of the present study was to identify differences in renal gene regulation that may affect kidney function and fluid balance, which could contribute to decompensation in Balb/CJ mice after ANG II + salt treatment.
View Article and Find Full Text PDFGhrelin Ameliorates Angiotensin II-Induced Myocardial Fibrosis by Upregulating Peroxisome Proliferator-Activated Receptor Gamma in Young Male Rats.
Biomed Res Int
December 2018
Department of Cardiology, China-Japan Union Hospital, Jilin University, Changchun 130033, China.
Angiotensin (Ang) II contributes to the formation and development of myocardial fibrosis. Ghrelin, a gut peptide, has demonstrated beneficial effects against cardiovascular disease. In the present study, we explored the effect and related mechanism of Ghrelin on myocardial fibrosis in Ang II-infused rats.
View Article and Find Full Text PDFInhibitory effects of low decibel infrasound on the cardiac fibroblasts and the involved mechanism.
Noise Health
August 2017
Department of Cardiology, Third Hospital of Nanchang, Nanchang, China.
Introduction: Infrasound is a mechanical vibration wave with frequency between 0.0001 and 20 Hz. It has been established that infrasound of 120 dB or stronger is dangerous to humans.
View Article and Find Full Text PDFAmlodipine suppresses Ang-II-induced endothelium dysfunction by diminishing ROCK1 expression.
Clin Exp Hypertens
October 2016
a Department of Cardiology , The First Affiliated Hospital of Sun Yat-sen University, Guangzhou , China and.
Objective: To investigate the effects and mechanisms of amlodipine therapy on endothelium dysfunction induced by angiotensin-II (Ang-II) stimulation.
Methods: Human umbilical vein endothelial cells (HUVECs) were used and divided into five groups: Blank control, Ang-II (10(-6 )mol/L), levorotatory amlodipine (5 × 10(-6 )mol/L) + Ang-II (10(-6 )mol/L), dextrorotatory amlodipine (5 × 10(-6 )mol/L) + Ang-II (10(-6 )mol/L) and racemic amlodipine (5 × 10(-6 )mol/L) + Ang-II (10(-6 )mol/L) groups. Twenty-four hours later, HUVECs were collected for evaluating endothelial nitric oxide synthase (eNOS), p-eNOS, rho-associated kinase 1 (ROCK1), Bcl-2 and Bax expressions.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!