scholarly journals Cardiovascular actions of chicken-meat extract in normo- and hypertensive rats

2001 ◽  
Vol 86 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Meng-Kwoon Slim
Keyword(s):  
Cardiac Hypertrophy ◽  
Treatment Period ◽  
Chicken Meat ◽  
Oral Feeding ◽  
Hypertensive Rats ◽  
Meat Extract ◽  
Cardiovascular Actions ◽  
Age Related ◽  
Related Development ◽  
Experimentally Induced

The cardiovascular actions of a commercial chicken-meat extract known as Brand's Essence of Chicken (Cerebos Pacific Ltd, Singapore; BEC) were investigated in normo- and hypertensive rats. The spontaneously-hypertensive rat (SHR), Wistar Kyoto rat (WKY) and Sprague Dawley rat (SD) were used. The effect of oral feeding of BEC on hypertension, cardiac hypertrophy and arteriosclerosis in these animals was studied. The data showed the following effects of oral feeding of BEC: (1) feeding for 30 d did not affect the blood pressure and heart rate (determined telemetrically) of adult SHR and WKY; (2) feeding for 90 d did not affect the development of hypertension in 1-month-old prehypertensive SHR; (3) feeding for 4 d dose-dependently (0·2–3·2 ml/kg per d) attenuated cardiac hypertrophy in experimentally-induced (coarctation of the abdominal aorta) cardiac hypertrophic SD; (4) feeding to 1-month-old prehypertensive SHR for 11 months did not affect the age-related development of hypertension in this animal; (5) there was significant attenuation of the age-related development of hypertension (determined by tail-cuff plethysmography) in the WKY (P=0·011) when the animals drank an average of 7·5 ml BEC/kg body weight per d, measured during the last 2 months of the 11-month treatment period; (6) there was chronic, as in the previous treatment, attenuation of the age-related development of cardiac hypertrophy and arteriosclerosis (quantified morphometrically) in the SHR when the animals drank an average of 2·4 ml BEC/kg per d, measured during the last 2 months of the 11-month treatment period. A parallel study using laboratory-prepared chicken-meat and pork extracts showed that the former, but not the latter, attenuated cardiac hypertrophy in experimentally-induced cardiac hypertrophic SD. These findings, showing that chicken-meat extract (both BEC and laboratory prepared) could have anti-cardiac hypertrophic, anti-hypertensive and anti-arteriosclerotic actions, were unexpected and provoking, and would challenge nutritional scientists with an interest in meat consumption and cardiovascular diseases.

scholarly journals Continuous Blockade of L-Type Ca2+ Channels Suppresses Activation of Calcineurin and Development of Cardiac Hypertrophy in Spontaneously Hypertensive Rats

2002 ◽  
Vol 25 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Yunzeng ZOU ◽  
Tsutomu YAMAZAKI ◽  
Keiichi NAKAGAWA ◽  
Haruyasu YAMADA ◽  
Norio IRIGUCHI ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ca2 Channels

scholarly journals Change by challenge: A common genetic basis behind childhood cognitive development and cognitive training

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Bruno Sauce ◽  
John Wiedenhoeft ◽  
Nicholas Judd ◽  
Torkel Klingberg
Keyword(s):  
Cognitive Development ◽  
Brain Plasticity ◽  
Training Sample ◽  
Age Related ◽  
Central Piece ◽  
Gene Environment ◽  
Related Development ◽  
Explained Variation ◽  
Genetic And Environmental Factors ◽  
Cognitive Challenges

AbstractThe interplay of genetic and environmental factors behind cognitive development has preoccupied multiple fields of science and sparked heated debates over the decades. Here we tested the hypothesis that developmental genes rely heavily on cognitive challenges—as opposed to natural maturation. Starting with a polygenic score (cogPGS) that previously explained variation in cognitive performance in adults, we estimated its effect in 344 children and adolescents (mean age of 12 years old, ranging from 6 to 25) who showed changes in working memory (WM) in two distinct samples: (1) a developmental sample showing significant WM gains after 2 years of typical, age-related development, and (2) a training sample showing significant, experimentally-induced WM gains after 25 days of an intense WM training. We found that the same genetic factor, cogPGS, significantly explained the amount of WM gain in both samples. And there was no interaction of cogPGS with sample, suggesting that those genetic factors are neutral to whether the WM gains came from development or training. These results represent evidence that cognitive challenges are a central piece in the gene-environment interplay during cognitive development. We believe our study sheds new light on previous findings of interindividual differences in education (rich-get-richer and compensation effects), brain plasticity in children, and the heritability increase of intelligence across the lifespan.

scholarly journals Dill Extract Induces Elastic Fiber Neosynthesis and Functional Improvement in the Ascending Aorta of Aged Mice with Reversal of Age-Dependent Cardiac Hypertrophy and Involvement of Lysyl Oxidase-Like-1

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 173 ◽  
Author(s):  
Wassim Fhayli ◽  
Quentin Boëté ◽  
Nadjib Kihal ◽  
Valérie Cenizo ◽  
Pascal Sommer ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Lysyl Oxidase ◽  
Elastic Fiber ◽  
Ascending Aorta ◽  
Functional Improvement ◽  
Elastic Fibers ◽  
Aged Mice ◽  
Age Related ◽  
And Function

Elastic fibers (90% elastin, 10% fibrillin-rich microfibrils) are synthesized only in early life and adolescence mainly by the vascular smooth muscle cells through the cross-linking of its soluble precursor, tropoelastin. Elastic fibers endow the large elastic arteries with resilience and elasticity. Normal vascular aging is associated with arterial remodeling and stiffening, especially due to the end of production and degradation of elastic fibers, leading to altered cardiovascular function. Several pharmacological treatments stimulate the production of elastin and elastic fibers. In particular, dill extract (DE) has been demonstrated to stimulate elastin production in vitro in dermal equivalent models and in skin fibroblasts to increase lysyl oxidase–like-1 (LOXL-1) gene expression, an enzyme contributing to tropoelastin crosslinking and elastin formation. Here, we have investigated the effects of a chronic treatment (three months) of aged male mice with DE (5% or 10% v/v, in drinking water) on the structure and function of the ascending aorta. DE treatment, especially at 10%, of aged mice protected pre-existing elastic lamellae, reactivated tropoelastin and LOXL-1 expressions, induced elastic fiber neo-synthesis, and decreased the stiffness of the aging aortic wall, probably explaining the reversal of the age-related cardiac hypertrophy also observed following the treatment. DE could thus be considered as an anti-aging product for the cardiovascular system.

Role of sympathetic nerves during developing cardiac hypertrophy in Grollman hypertensive rats

1987 ◽  
Vol 253 (4) ◽  
pp. H818-H825
Author(s):  
R. J. Tomanek ◽  
D. W. Carlson ◽  
P. J. Palmer ◽  
R. K. Bhatnagar
Keyword(s):  
Cardiac Hypertrophy ◽  
Renovascular Hypertension ◽  
Volume Expansion ◽  
Peripheral Resistance ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Lv Function ◽  
Hypertensive Rats ◽  
Anterior Portion ◽  
Mitochondrial Volume

Peak left ventricular (LV) function, during rapid volume expansion, and cardiocyte structure were studied in rats with developing cardiac hypertrophy in response to Grollman hypertension (1 kidney, 1 figure 8) after chemical sympathectomy with 6-hydroxydopamine. This form of renovascular hypertension led to the same magnitude of hypertrophy in rats with or without sympathectomy. Indices of peak LV function, measured during acute volume expansion, tended to be normal or slightly higher in hypertensive rats than in controls. Sympathectomy in rats with hypertension significantly improved cardiac and stroke indices while decreasing total peripheral resistance at peak cardiac output. Despite similar magnitudes of LV hypertrophy (LVH) in the two hypertensive groups, cardiocytes in sympathectomized rats had higher mitochondrial volume densities and slightly lower myofibrillar volume densities. After regional sympathectomy of the anterior portion of the LV with phenol, mitochondrial volume density increased by 21% in hypertensive rats with LVH. These data indicate that, during the development of LVH in response to renovascular hypertension, sympathetic nerves do not contribute to the magnitude of LVH but may limit improvement in peak LV performance in response to increased preload. However, sympathetic nerves do play a role in the regulation of mitochondrial and myofibril growth.

Alteration of Atrial Natriuretic Peptide and Brain Natriuretic Peptide Gene Expression Associated with Progression and Regression of Cardiac Hypertrophy in Renovascular Hypertensive Rats

1996 ◽  
Vol 90 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Hideo Kawakami ◽  
Hideki Okayama ◽  
Mareomi Hamada ◽  
Kunio Hiwada
Keyword(s):  
Gene Expression ◽  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Regression Of Cardiac Hypertrophy ◽  
Peptide Gene ◽  
Atrial Natriuretic

1. We assessed the changes of atrial natriuretic peptide and brain natriuretic peptide gene expression associated with progression and regression of cardiac hypertrophy in renovascular hypertensive rats (RHR). 2. Two-kidney, one-clip hypertensive rats (6-week-old male Wistar) were made and studied 6 (RHR-1) and 10 weeks (RHR-2) after the procedure. Regression of cardiac hypertrophy was induced by nephrectomy at 6 weeks after constriction, and the nephrectomized rats were maintained further for 4 weeks (nephrectomized rat: NEP). Sham operation was performed, and the rats were studied after 6 (Sham-1) and 10 weeks (Sham-2). Atrial natriuretic peptide and brain natriuretic peptide gene expression in the left ventricle was analysed by Northern blotting. 3. Plasma atrial natriuretic peptide and brain natriuretic peptide were significantly higher in RHR-1 and RHR-2 than in Sham-1, Sham-2 and NEP. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels in RHR-1 were approximately 7.2-fold and 1.8-fold higher than those in Sham-1, respectively, and the corresponding levels in RHR-2 were 13.0-fold and 2.4-fold higher than those in Sham-2, respectively. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels of NEP were normalized. Levels of atrial natriuretic peptide and brain natriuretic peptide mRNA were well correlated positively with left ventricular weight/body weight ratios. There was a significant positive correlation between the levels of atrial natriuretic peptide and brain natriuretic peptide mRNA (r = 0.86, P<0.01). 4. We conclude that the expression of atrial natriuretic peptide and brain natriuretic peptide genes is regulated in accordance with the degree of myocardial hypertrophy and that the augmented expression of these two natriuretic peptides may play an important role in the maintenance of cardiovascular haemodynamics in renovascular hypertension.

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