Myocardial remodeling in SHR rats with age-related hypertrophy was characterized by elimination of cardiomyocytes, their hypertrophy, and marked increase in the volume of the connective tissue. The count of cardiomyocytes with contracture injuries and subsegmental contractures increased, and pronounced perivascular and interstitial sclerosis developed in the hypertrophic myocardium of SHR rats. Damage to the microcirculatory bed manifested in degenerative changes and destruction of some endotheliocytes. Signs of atypical intracellular regeneration in myofibrils and impairment of their longitudinal orientation were revealed in cardiomyocytes in the late stage of compensatory hypertrophy.
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http://dx.doi.org/10.1023/a:1023836318560 | DOI Listing |
Mol Imaging Biol
January 2025
Molecular Imaging Chemistry Laboratory, Wolfson Brain Imaging Centre, Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK.
Purpose: Positron Emission Tomography (PET) scans with radioligands targeting tau neurofibrillary tangles (NFT) have accelerated our understanding of the role of misfolded tau in neurodegeneration. While intended for human research, applying these radioligands to small animals establishes a vital translational link. Transgenic animal models of dementia, such as the tau rat SHR24, play a crucial role in enhancing our understanding of these disorders.
View Article and Find Full Text PDFReceptors for the vasoactive adipokine apelin, termed APJ receptors, are G-protein-coupled receptors and are widely expressed throughout the cardiovascular system. APJ receptors can also signal via G-protein-independent pathways, including G-protein-coupled-receptor kinase 2 (GRK2), which inhibits nitric oxide synthase (eNOS) activity and nitric oxide (NO) production in endothelial cells. Apelin causes endothelium-dependent, NO-mediated relaxation of coronary arteries from normotensive animals, but the effects of activating APJ receptor signaling pathways in hypertensive coronary arteries are largely unknown.
View Article and Find Full Text PDFBehav Brain Res
January 2025
Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Unidad Tlaxcala, Mexico. Electronic address:
Hypertension, if untreated, can disrupt the blood-brain-barrier (BBB) and reduce cerebral flow in the central nervous system (CNS) inducing hippocampal atrophy, potentially leading to cognitive deficits and vascular dementia. Spontaneous hypertensive rats (SHR) demonstrated neuroplastic alterations in the hippocampus, hyperlocomotion and memory deficits in males. Cerebrolysin (CBL), a neuropeptide preparation, induces synaptic and neuronal plasticity in various populations of neurons and repairs the integrity of the BBB.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
January 2025
College of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Objectives: To explore the mechanism of Granules (QDG) for alleviating brain damage in spontaneously hypertensive rats (SHRs).
Methods: Twelve 5-week-old SHRs were randomized into SHR control group and SHR+QDG group treated with QDG by gavage at the daily dose of 0.9 g/kg for 12 weeks.
J Recept Signal Transduct Res
January 2025
Department of Pharmaceutical Sciences, Barry and Judy Silverman College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL, USA.
The proliferative effects of angiotensin (Ang) II in vascular smooth muscle cells (VSMCs) through its ability to stimulate extracellular signal-regulated kinases 1 and 2 (ERK1/2) pathway have been established. The main goal of this study was to explore whether Ang III induces ERK1/2 MAPK and VSMC proliferation in cultured Wistar VSMCs. Further, the Ang III actions were compared to those observed in VSMCs derived from the spontaneously hypertensive rat (SHR).
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