The role of (pro)rennin receptor (PRR) in cardiomyocytes of a heart failure (HF) rat model was studied. Spontaneously hypertensive rats (SHR) with HF (SHR-HF) or not were identified by two-dimensional (2-D) ultrasound. Age-matched Wistar Kyoto normotensive (WKY) rats were used as controls. PRR short hair RNA (sh-RNA) was injected into the heart of SHR-HF. Simultaneously SHR and controls received the same shRNA injection into the heart. Scramble shRNA was injected into the heart as controls. The expression of PRR mRNA and protein in cardiomyocytes was detected by using real-time PCR and Western blotting respectively. The heart function was evaluated by 2-D ultrasound, including eject fraction (EF%), fractional shortening (FS%), left ventricle thickness (LV), and inter-ventricular septal thickness (IVS). The number of apoptotic cardiomyocytes was counted by using flow cytometry. The results showed that the mRNA and protein expression levels of PRR were significantly higher in cardiomyocytes of SHR-HF group than in those of SHR group or control group. The apoptosis of myocytes in SHR-HF group was increased as compared with SHR group or control group. After knock-down of PRR with shRNA in SHR-HF group, the apoptosis of myocytes was reduced, resulting in the improved heart function. It was suggested that down-regulation of PRR might protect the heart from development of HF in SHR-HF by inhibiting the apoptosis of cardiomyocytes.
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http://dx.doi.org/10.1007/s11596-013-1173-0 | DOI Listing |
J Mol Cell Cardiol
January 2018
Institute of Pharmacology and Clinical Pharmacy, Biochemical and Pharmacological Center (BPC) Marburg, University of Marburg, Karl-von-Frisch-Str. 1, D-35032 Marburg, Germany. Electronic address:
Hypertensive heart disease (HHD) can cause left ventricular (LV) hypertrophy and heart failure (HF). It is unclear, though, which factors may contribute to the transition from compensated LV hypertrophy to HF in HHD. We hypothesized that maladaptive atrial remodeling with impaired atrial myocyte function would occur in advanced HHD and may be associated with the emergence of HF.
View Article and Find Full Text PDFJ Huazhong Univ Sci Technolog Med Sci
October 2013
Department of Ultrosound, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
The role of (pro)rennin receptor (PRR) in cardiomyocytes of a heart failure (HF) rat model was studied. Spontaneously hypertensive rats (SHR) with HF (SHR-HF) or not were identified by two-dimensional (2-D) ultrasound. Age-matched Wistar Kyoto normotensive (WKY) rats were used as controls.
View Article and Find Full Text PDFAm J Hypertens
July 2011
Department of Pharmacology & Toxicology and Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Background: Angiotensin receptor blockers (ARB), telmisartan, and valsartan were compared for renal protection in spontaneously hypertensive rats (SHR) fed high fat diet. We hypothesized that in cardiometabolic syndrome, telmisartan an ARB with peroxisome proliferators activated receptor-γ (PPAR-γ) activity will offer better renal protection.
Methods: SHR were fed either normal (SHR-NF, 7% fat) or high fat (SHR-HF, 36% fat) diet and treated with an ARB for 10 weeks.
Nephrol Dial Transplant
February 2010
Division of Nephrology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Background: Obesity has been strongly associated with the development and aggravation of hypertension and chronic kidney disease. To date, the systemic renin-angiotensin system (RAS) has been known to involve in obesity-induced tissue damage and hypertension. However, the intrarenal mechanism whereby obesity induces and aggravates hypertension and renal disease remains poorly understood.
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