Ouabain Attenuates Cardiac Hypertrophy of Male Rat Offspring Exposed to Intrauterine Growth Restriction Following High-Salt Diet Challenge

2015 ◽  
Vol 22 (12) ◽  
pp. 1587-1596 ◽  
Author(s):  
Liang Chen ◽  
Jing Yue ◽  
Han Wu ◽  
Jun Yang ◽  
Xiaojuan Han ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Intrauterine Growth Restriction ◽  
High Salt ◽  
Growth Restriction ◽  
Male Rat ◽  
High Salt Diet ◽  
Salt Diet ◽  
Intrauterine Growth ◽  
Rat Offspring

Maternal high-salt diet altered PKC/MLC20 pathway and increased ANG II receptor-mediated vasoconstriction in adult male rat offspring

2016 ◽  
Vol 60 (7) ◽  
pp. 1684-1694 ◽  
Author(s):  
Weisheng Li ◽  
Juanxiu Lv ◽  
Jue Wu ◽  
Xiuwen Zhou ◽  
Lin Jiang ◽  
...  
Keyword(s):  
Adult Male ◽  
High Salt ◽  
Male Rat ◽  
Ang Ii ◽  
High Salt Diet ◽  
Salt Diet ◽  
Rat Offspring ◽  
Adult Male Rat

scholarly journals AT1 receptor participates in the cardiac hypertrophy induced by resistance training in rats

2008 ◽  
Vol 295 (2) ◽  
pp. R381-R387 ◽  
Author(s):  
Valerio G. Barauna ◽  
Flávio C. Magalhaes ◽  
Jose E. Krieger ◽  
Edilamar M. Oliveira
Keyword(s):  
Resistance Training ◽  
Left Ventricle ◽  
Cardiac Hypertrophy ◽  
Receptor Gene ◽  
Weight Ratio ◽  
High Salt ◽  
Receptor Expression ◽  
Ang Ii ◽  
High Salt Diet ◽  
Salt Diet

Resistance training is accompanied by cardiac hypertrophy, but the role of the renin-angiotensin system (RAS) in this response is elusive. We evaluated this question in 36 male Wistar rats divided into six groups: control ( n = 6); trained ( n = 6); control + losartan (10 mg·kg−1·day−1, n = 6); trained + losartan ( n = 6); control + high-salt diet (1%, n = 6); and trained + high-salt diet (1%, n = 6). High salt was used to inhibit the systemic RAS and losartan to block the AT1 receptor. The exercise protocol consisted of: 4 × 12 bouts, 5×/wk during 8 wk, with 65–75% of one repetition maximum. Left ventricle weight-to-body weight ratio increased only in trained and trained + high-salt diet groups (8.5% and 10.6%, P < 0.05) compared with control. Also, none of the pathological cardiac hypertrophy markers, atrial natriuretic peptide, and αMHC (α-myosin heavy chain)-to-βMHC ratio, were changed. ACE activity was analyzed by fluorometric assay (systemic and cardiac) and plasma renin activity (PRA) by RIA and remained unchanged upon resistance training, whereas PRA decreased significantly with the high-salt diet. Interestingly, using Western blot analysis and RT-PRC, no changes were observed in cardiac AT2 receptor levels, whereas the AT1 receptor gene (56%, P < 0.05) and protein (31%, P < 0.05) expressions were upregulated in the trained group. Also, cardiac ANG II concentration evaluated by ELISA remained unchanged (23.27 ± 2.4 vs. 22.01 ± 0.8 pg/mg, P > 0.05). Administration of a subhypotensive dose of losartan prevented left ventricle hypertrophy in response to the resistance training. Altogether, we provide evidence that resistance training-induced cardiac hypertrophy is accompanied by induction of AT1 receptor expression with no changes in cardiac ANG II, which suggests a local activation of the RAS consistent with the hypertrophic response.

scholarly journals Salt-sensitive hypertension and cardiac hypertrophy in mice deficient in the ubiquitin ligase Nedd4-2

2008 ◽  
Vol 295 (2) ◽  
pp. F462-F470 ◽  
Author(s):  
Peijun P. Shi ◽  
Xiao R. Cao ◽  
Eileen M. Sweezer ◽  
Thomas S. Kinney ◽  
Nathan R. Williams ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Critical Role ◽  
Specific Inhibitor ◽  
Normal Diet ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Ww Domains ◽  
Salt Sensitive Hypertension

Nedd4-2 has been proposed to play a critical role in regulating epithelial Na+ channel (ENaC) activity. Biochemical and overexpression experiments suggest that Nedd4-2 binds to the PY motifs of ENaC subunits via its WW domains, ubiquitinates them, and decreases their expression on the apical membrane. Phosphorylation of Nedd4-2 (for example by Sgk1) may regulate its binding to ENaC, and thus ENaC ubiquitination. These results suggest that the interaction between Nedd4-2 and ENaC may play a crucial role in Na+ homeostasis and blood pressure (BP) regulation. To test these predictions in vivo, we generated Nedd4-2 null mice. The knockout mice had higher BP on a normal diet and a further increase in BP when on a high-salt diet. The hypertension was probably mediated by ENaC overactivity because 1) Nedd4-2 null mice had higher expression levels of all three ENaC subunits in kidney, but not of other Na+ transporters; 2) the downregulation of ENaC function in colon was impaired; and 3) NaCl-sensitive hypertension was substantially reduced in the presence of amiloride, a specific inhibitor of ENaC. Nedd4-2 null mice on a chronic high-salt diet showed cardiac hypertrophy and markedly depressed cardiac function. Overall, our results demonstrate that in vivo Nedd4-2 is a critical regulator of ENaC activity and BP. The absence of this gene is sufficient to produce salt-sensitive hypertension. This model provides an opportunity to further investigate mechanisms and consequences of this common disorder.

Alterations in apoptosis regulatory factors during hypertrophy and heart failure

2004 ◽  
Vol 287 (1) ◽  
pp. H72-H80 ◽  
Author(s):  
Peter M. Kang ◽  
Patrick Yue ◽  
Zhilin Liu ◽  
Oleg Tarnavski ◽  
Natalya Bodyak ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Primary Cultures ◽  
High Salt ◽  
Terminal Deoxynucleotidyl Transferase ◽  
High Salt Diet ◽  
Salt Diet ◽  
Pathological Hypertrophy ◽  
Increased Sensitivity ◽  
Physiological Hypertrophy

Cardiac hypertrophy from pathological stimuli often proceeds to heart failure, whereas cardiac hypertrophy from physiological stimuli does not. In this study, physiological hypertrophy was created by a daily exercise regimen and pathological hypertrophy was created from a high-salt diet in Dahl salt-sensitive rats. The rats continued on a high-salt diet progressed to heart failure associated with an increased rate of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cardiomyocytes. We analyzed primary cultures of these hearts and found that only cardiomyocytes made hypertrophic by a pathological stimulus show increased sensitivity to apoptosis. Examination of the molecular changes associated with these distinct types of hypertrophy revealed changes in Bcl-2 family members and caspases favoring survival during physiological hypertrophy. However, in pathological hypertrophy, there were more diffuse proapoptotic changes, including changes in Fas, the Bcl-2 protein family, and caspases. Therefore, we speculate that this increased sensitivity to apoptotic stimulation along with proapoptotic changes in the apoptosis program may contribute to the development of heart failure seen in pathological cardiac hypertrophy.

scholarly journals Oxidative Stress and Neurodevelopmental Outcomes in Rat Offspring with Intrauterine Growth Restriction Induced by Reduced Uterine Perfusion

2021 ◽  
Vol 11 (1) ◽  
pp. 78
Author(s):  
Marcelo E. Rains ◽  
Colin B. Muncie ◽  
Yi Pang ◽  
Lir-Wan Fan ◽  
Lu-Tai Tien ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Oxidative Stress Markers ◽  
Neurodevelopmental Outcomes ◽  
Pregnant Rats ◽  
Intrauterine Growth ◽  
Rat Offspring ◽  
Stress Markers ◽  
Uterine Perfusion

Intrauterine growth restriction (IUGR) is a major cause of morbidity and mortality and is worldwide associated with delayed neurodevelopment. The exact mechanism involved in delayed neurodevelopment associated with IUGR is still unclear. Reduced uterine perfusion (RUP) is among the main causes of placental insufficiency leading to IUGR, which is associated with increases in oxidative stress. This study investigated whether oxidative stress is associated with delayed neurodevelopment in IUGR rat pups. Pregnant rats were exposed to RUP surgery on gestational day 14 to generate IUGR rat offspring. We evaluated offspring’s morphometric at birth, and neurodevelopment on postnatal day 21 (PD21) as well as markers of oxidative stress in plasma and brain. Offspring from dams exposed to RUP showed significant (p < 0.05) lower birth weight compared to controls, indicating IUGR. Motor and cognitive deficits, and levels of oxidative stress markers, were significantly (p < 0.05) elevated in IUGR offspring compared to controls. IUGR offspring showed significant (p < 0.05) negative correlations between brain lipid peroxidation and neurocognitive tests (open field and novel object recognition) in comparison with controls. Our findings suggest that neurodevelopmental delay observed in IUGR rat offspring is associated with increased levels of oxidative stress markers.

scholarly journals Intrauterine growth restriction inhibits cell proliferation within the subventricular zone and white matter of rat offspring

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Leigh Rhodes Campbell ◽  
Baoying Zheng ◽  
Norma B Ojeda ◽  
Thomas P Royals ◽  
Philip G Rhodes ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
White Matter ◽  
Subventricular Zone ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Rat Offspring
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