Relationship between dietary sodium intake, hemodynamics, and cardiac mass in SHR and WKY rats

Fröhlich, Edward D.; Chien, Y.W.; Shoji, Shuichi; Pegram, Barbara L.

doi:10.1152/ajpregu.1993.264.1.r30

Cited by 76 publications

(97 citation statements)

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“…In cultured neonatal rat myocardial myoblasts, cellular protein content and cell size increased when sodium concentration of the medium was augmented (15). In vivo, a high-sodium intake increased cardiac mass in normotensive rats (46) and exacerbated cardiac hypertrophy in hypertensive rats (12). In humans, sodium intake (assessed by urinary sodium excretion) and the left ventricular mass index were positively correlated in hypertensive and normotensive subjects (9).…”

mentioning

confidence: 98%

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Rugale¹,

Delbosc

Cristol

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Rugale, Caroline, Sandrine Delbosc, Jean-Paul Cristol, Albert Mimran, and Bernard Jover. Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension. Am J Physiol Heart Circ Physiol 284: H1744-H1750, 2003. First published December 5, 2002 10.1152/ajpheart.00864.2002The influence of a low-sodium (LS) diet was assessed on the cardiac and renal alterations and pro-oxidant effect associated with a 10-day infusion of angiotensin II (200 or 400 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 , osmotic pumps). Tail-cuff pressure (TCP), albuminuria, and renal blood flow were determined at the end of the experiments. Heart weight index (HWI) and production of superoxide anion (O 2 Ϫ ⅐) by the left ventricle and H2O2 by the aorta was measured with the use of bioluminescence. Although the final TCP was similar in LS and normal sodium (NS) rats infused with high and low doses of angiotensin II, respectively, the increase in HWI was prevented by the LS diet. Sodium restriction reduced the rise in albuminuria without a change in the renal effect of angiotensin II. The increased production of O 2 Ϫ ⅐ and H2O2 observed in NS rats was abrogated in LS rats. The beneficial influence of dietary sodium restriction on target organ damage induced by angiotensin II is independent of arterial pressure reduction and possibly related to attenuation of the prooxidant effect of the peptide. heart weight; albuminuria; reactive oxygen species; renal hemodynamic THE DEVELOPMENT OF cardiac hypertrophy results from the interaction between several factors, including elevated arterial pressure, angiotensin II (ANG II), and sodium intake. Although blood pressure is an important determinant of cardiac mass (8), ANG II may directly increase protein synthesis and cause myocyte hypertrophy, as reported in cultured cardiac myocytes isolated from chicks (2) and neonatal rats (34). In vivo long-term administration of an initially subpressor dose of ANG II, a model that mimics the development of human hypertension, induces a gradual rise in blood pressure associated with a cardiac hypertrophy (7,14,17). However, ANG II might increase cardiac mass independently of arterial pressure. This was suggested by the presence of cardiac hypertrophy in rats infused with a nonpressor dose of the peptide (4, 37) or in rats infused with a pressor dose of ANG II and concomitantly treated by hydralazine (7, 37).The concentration of sodium ion in vitro or dietary sodium intake in vivo may modulate cardiac mass. In cultured neonatal rat myocardial myoblasts, cellular protein content and cell size increased when sodium concentration of the medium was augmented (15). In vivo, a high-sodium intake increased cardiac mass in normotensive rats (46) and exacerbated cardiac hypertrophy in hypertensive rats (12). In humans, sodium intake (assessed by urinary sodium excretion) and the left ventricular mass index were positively correlated in hypertensive and normotensive subjects (9). Conversely, a low-sodium (LS) intake prevents cardiac hypertrophy associated with two-k...

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mentioning

confidence: 98%

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Rugale¹,

Delbosc

Cristol

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…Changes in the distribution of HDAC4, HDAC5, and HDAC7 have been observed during mitosis, including the exclusion of HDAC4 from condensed chromatin regions (128). Moreover, HDAC5 was shown to localize to the spindle midzone during mitosis and to the midbody during cytokinesis, where it interacts with the mitotic kinase Aurora B and is phosphorylated at S278 within the NLS (47) (Fig.…”

Section: Hdac5-although Numerous Hdac5mentioning

confidence: 99%

“…Along with changes in chromosome condensation status, histone acetylation levels have been shown to decrease early in mitosis, reaching their lowest levels during metaphase and anaphase, and rising at the late telophase/interphase transition (128). Additionally, global inhibition of HDACs using small molecules has been shown to inhibit mitotic progression by inducing G2-phase checkpoint response (129,130).…”

Section: Hdac5-although Numerous Hdac5mentioning

confidence: 99%

“…Export of HDAC5, and subsequent MEF2 activation, can also be triggered by nuclear GRK5 under hypertensive conditions, leading to ventricular hypertrophy (124,143). Independently of blood pressure, high salt intake has also been known to be associated with left ventricle hypertrophy (128,144). More recently, this mechanism was shown to be phosphorylation-dependent, as increased sodium levels activate the critical cardiac kinase SIK1, leading to HDAC5 phosphorylation and enhanced MEF2 and NFAT transcriptional activity (72).…”

Section: Hdac5-although Numerous Hdac5mentioning

confidence: 99%

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Post-translational Modifications Regulate Class IIa Histone Deacetylase (HDAC) Function in Health and Disease

Mathias

Guise

Cristea

2015

Molecular & Cellular Proteomics

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Class IIa histone deacetylases (HDACs4, -5, -7, and -9) modulate the physiology of the human cardiovascular, musculoskeletal, nervous, and immune systems. The regulatory capacity of this family of enzymes stems from their ability to shuttle between nuclear and cytoplasmic compartments in response to signal-driven post-translational modification. Here, we review the current knowledge of modifications that control spatial and temporal histone deacetylase functions by regulating subcellular localization, transcriptional functions, and cell cycle-dependent activity, ultimately impacting on human disease. We discuss the contribution of these modifications to cardiac and vascular hypertrophy, myoblast differentiation, neuronal cell survival, and neurodegenerative disorders. Molecular & Cellular

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“…O sal tem uma ação na estrutura cardíaca (Fröhlich et al, 1993) e que 9,5% da mortalidade da população mundial por doenças cardiovasculares é decorrente do excesso do consumo de sal (Mozaffarian et al,2014).…”

Section: Resultsunclassified

Sobrecarga e restrição de cloreto de sódio durante a gestação: repercussão sobre a estrutura cardíaca e renal no neonato

Nogueira¹

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AGRADECIMENTOSAgradeço primeiramente a Deus qυе iluminou о mеυ caminho durante este projeto e também agradeço a Nossa Senhora de Aparecida pela intercessão das graças recebidas.À minha família que nesta trajetória foi essencial pelo apoio incondicional e sacrifício imposto pela distância.Ao meu esposo Rodrigo, muito obrigada pelo carinho, pela paciência e por sua capacidade de me trazer a paz na correria diária. Você é uma pessoa incrível.À minha mãe Edite, um grande exemplo de mulher que superou as dificuldades da saúde para continuar me dando forças. Uma figura importantíssima na minha vida, uma mulher que sozinha buscou o melhor para suas filhas. Tenho muito orgulho de ser sua filha.À minha irmã querida, pelo apoio e carinho.À minha prima Carolina Rivas, pela força, pelo companheirismo de todos os dias durante esses três anos.Em especial, quero agradecer meu orientador Dr. Joel Claudio Heimann, um grande profissional ético e dedicado no seu trabalho árduo e contínuo. Tenho uma imensa gratidão por ter me recebido no seu grupo de pesquisa e ter acreditado em mim. Muito obrigada por estar sempre comigo nesta trajetória, seja no choro ou no riso, pelos ouvidos sempre disponíveis, pela cumplicidade e principalmente pela paciência. Por dizer-me não somente o que quero ouvir, mas As secretarias Solange e Denise.Aos técnicos e auxiliares, Janice, Claudia, Meire e Newton.À coordenação de pós-graduação.À FAPESP e a CAPES pelo apoio financeiro.

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Relationship between dietary sodium intake, hemodynamics, and cardiac mass in SHR and WKY rats

Cited by 76 publications

References 0 publications

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Post-translational Modifications Regulate Class IIa Histone Deacetylase (HDAC) Function in Health and Disease

Sobrecarga e restrição de cloreto de sódio durante a gestação: repercussão sobre a estrutura cardíaca e renal no neonato

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