Estrogen delays the progression of salt-induced cardiac hypertrophy by influencing the renin-angiotensin system in heterozygous proANP gene-disrupted mice

S Jeson Sangaralingham, M. Yat Tse, Stephen C. Pang

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Left ventricular hypertrophy is considered an independent risk factor for cardiac morbidity and mortality, and many studies have shown that women have a lower incidence of left ventricular hypertrophy even after correcting for numerous risk factors. This cardio-protective effect seen in women has been attributed to estrogen, which likely modulates specific growth-promoting systems such as the renin-angiotensin system, and in turn may lead to the prevention of left ventricular hypertrophy. Furthermore, the underlying mechanisms responsible are poorly understood. The aim of the present study was to examine the effect of estrogen in relation to its impact on the development of left ventricular hypertrophy through its interaction with the renin-angiotensin system by using the pro ANP heterozygous (ANP +/-) mouse as a model of salt-sensitive cardiac hypertrophy. Male, female ANP +/- mice and also ovariectomized female ANP +/- mice treated with oil or estrogen, were fed either a normal or high-salt diet. All four groups exhibited a general suppression of the renin-angiotensin system under the high salt challenge. However, after the 5-week treatment period, marked left ventricular hypertrophy was noted only in the male and oil-injected ovariectomized female ANP +/- mice treated with high salt. Collectively, we provide direct evidence that the differences in cardiac hypertrophy between genders in ANP +/- mice is attributed to estrogen. Furthermore, estrogen may play a key role in slowing down the progression of salt-induced left ventricular hypertrophy in ANP +/- mice, in part, independent of the classical systemic renin-angiotensin system and possibly through other pathways.

Original languageEnglish (US)
Pages (from-to)221-230
Number of pages10
JournalMolecular and Cellular Biochemistry
Volume306
Issue number1-2
DOIs
StatePublished - Dec 2007
Externally publishedYes

Fingerprint

Angiotensins
Cardiomegaly
Atrial Natriuretic Factor
Renin-Angiotensin System
Renin
Left Ventricular Hypertrophy
Estrogens
Salts
Genes
Oils
Nutrition
Diet
Morbidity
Mortality
Incidence
Growth

Keywords

  • ANP gene-disruption
  • Cardiac hypertrophy
  • Dietary salt
  • Estrogen
  • Renin-angiotensin system

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

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title = "Estrogen delays the progression of salt-induced cardiac hypertrophy by influencing the renin-angiotensin system in heterozygous proANP gene-disrupted mice",
abstract = "Left ventricular hypertrophy is considered an independent risk factor for cardiac morbidity and mortality, and many studies have shown that women have a lower incidence of left ventricular hypertrophy even after correcting for numerous risk factors. This cardio-protective effect seen in women has been attributed to estrogen, which likely modulates specific growth-promoting systems such as the renin-angiotensin system, and in turn may lead to the prevention of left ventricular hypertrophy. Furthermore, the underlying mechanisms responsible are poorly understood. The aim of the present study was to examine the effect of estrogen in relation to its impact on the development of left ventricular hypertrophy through its interaction with the renin-angiotensin system by using the pro ANP heterozygous (ANP +/-) mouse as a model of salt-sensitive cardiac hypertrophy. Male, female ANP +/- mice and also ovariectomized female ANP +/- mice treated with oil or estrogen, were fed either a normal or high-salt diet. All four groups exhibited a general suppression of the renin-angiotensin system under the high salt challenge. However, after the 5-week treatment period, marked left ventricular hypertrophy was noted only in the male and oil-injected ovariectomized female ANP +/- mice treated with high salt. Collectively, we provide direct evidence that the differences in cardiac hypertrophy between genders in ANP +/- mice is attributed to estrogen. Furthermore, estrogen may play a key role in slowing down the progression of salt-induced left ventricular hypertrophy in ANP +/- mice, in part, independent of the classical systemic renin-angiotensin system and possibly through other pathways.",
keywords = "ANP gene-disruption, Cardiac hypertrophy, Dietary salt, Estrogen, Renin-angiotensin system",
author = "Sangaralingham, {S Jeson} and Tse, {M. Yat} and Pang, {Stephen C.}",
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T1 - Estrogen delays the progression of salt-induced cardiac hypertrophy by influencing the renin-angiotensin system in heterozygous proANP gene-disrupted mice

AU - Sangaralingham, S Jeson

AU - Tse, M. Yat

AU - Pang, Stephen C.

PY - 2007/12

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N2 - Left ventricular hypertrophy is considered an independent risk factor for cardiac morbidity and mortality, and many studies have shown that women have a lower incidence of left ventricular hypertrophy even after correcting for numerous risk factors. This cardio-protective effect seen in women has been attributed to estrogen, which likely modulates specific growth-promoting systems such as the renin-angiotensin system, and in turn may lead to the prevention of left ventricular hypertrophy. Furthermore, the underlying mechanisms responsible are poorly understood. The aim of the present study was to examine the effect of estrogen in relation to its impact on the development of left ventricular hypertrophy through its interaction with the renin-angiotensin system by using the pro ANP heterozygous (ANP +/-) mouse as a model of salt-sensitive cardiac hypertrophy. Male, female ANP +/- mice and also ovariectomized female ANP +/- mice treated with oil or estrogen, were fed either a normal or high-salt diet. All four groups exhibited a general suppression of the renin-angiotensin system under the high salt challenge. However, after the 5-week treatment period, marked left ventricular hypertrophy was noted only in the male and oil-injected ovariectomized female ANP +/- mice treated with high salt. Collectively, we provide direct evidence that the differences in cardiac hypertrophy between genders in ANP +/- mice is attributed to estrogen. Furthermore, estrogen may play a key role in slowing down the progression of salt-induced left ventricular hypertrophy in ANP +/- mice, in part, independent of the classical systemic renin-angiotensin system and possibly through other pathways.

AB - Left ventricular hypertrophy is considered an independent risk factor for cardiac morbidity and mortality, and many studies have shown that women have a lower incidence of left ventricular hypertrophy even after correcting for numerous risk factors. This cardio-protective effect seen in women has been attributed to estrogen, which likely modulates specific growth-promoting systems such as the renin-angiotensin system, and in turn may lead to the prevention of left ventricular hypertrophy. Furthermore, the underlying mechanisms responsible are poorly understood. The aim of the present study was to examine the effect of estrogen in relation to its impact on the development of left ventricular hypertrophy through its interaction with the renin-angiotensin system by using the pro ANP heterozygous (ANP +/-) mouse as a model of salt-sensitive cardiac hypertrophy. Male, female ANP +/- mice and also ovariectomized female ANP +/- mice treated with oil or estrogen, were fed either a normal or high-salt diet. All four groups exhibited a general suppression of the renin-angiotensin system under the high salt challenge. However, after the 5-week treatment period, marked left ventricular hypertrophy was noted only in the male and oil-injected ovariectomized female ANP +/- mice treated with high salt. Collectively, we provide direct evidence that the differences in cardiac hypertrophy between genders in ANP +/- mice is attributed to estrogen. Furthermore, estrogen may play a key role in slowing down the progression of salt-induced left ventricular hypertrophy in ANP +/- mice, in part, independent of the classical systemic renin-angiotensin system and possibly through other pathways.

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