Elevated dietary sodium intake exacerbates myocardial hypertrophy associated with cardiac-specific overproduction of angiotensin II

Porrello, Enzo R., Huggins, Catherine E., Curl, Claire L., Domenighetti, Andrea A., Pedrazzini, Thierry, Delbridge, Leanne M.D. and Morgan, Trefor O. 2004, Elevated dietary sodium intake exacerbates myocardial hypertrophy associated with cardiac-specific overproduction of angiotensin II, Journal of the renin-angiotensin-aldosterone system, vol. 5, no. 4, pp. 169-175, doi: 10.3317/jraas.2004.036.

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Title Elevated dietary sodium intake exacerbates myocardial hypertrophy associated with cardiac-specific overproduction of angiotensin II
Author(s) Porrello, Enzo R.
Huggins, Catherine E.
Curl, Claire L.
Domenighetti, Andrea A.
Pedrazzini, Thierry
Delbridge, Leanne M.D.
Morgan, Trefor O.
Journal name Journal of the renin-angiotensin-aldosterone system
Volume number 5
Issue number 4
Start page 169
End page 175
Publisher Sage
Place of publication Thousand Oaks, Calif.
Publication date 2004
ISSN 1470-3203
Summary Introduction/hypothesis
Cardiac hypertrophy is an independent risk factor predictive of cardiovascular disease and is significantly associated with morbidity and mortality. The mechanism by which angiotensin II (Ang II) and dietary sodium exert additive effects on the development of cardiac hypertrophy is unclear. The goal of this study was to evaluate the hypothesis that, where there is a genetic predisposition to Ang II-dependent hypertrophy, there is also an increased susceptibility to sodium-induced hypertrophy mediated by AT1-receptor expression.

Diets of low sodium (LS, 0.3% w:w) and high sodium (HS, 4.0% w:w) content were fed to adult (age 25 weeks) control wild-type mice (WT) and to weeks) control wild-type mice (WT) and to transgenic mice exhibiting cardiac specific overexpression of angiotensinogen (TG). At the conclusion of a 40-day dietary treatment period, cardiac tissue weights were compared and the relative expression levels of Ang II receptor subtypes (AT1A and AT2) were evaluated using RT-PCR.

WT and TG mice fed HS and LS diets maintained comparable weight gains during the treatment period. The normalised heart weights of TG mice were elevated compared to WT, and the extent of the increase was greater for mice maintained on the HS diet treatments (WT 12% vs. TG 41% increase in cardiac weight index). While a similar pattern of growth was observed for ventricular tissues, the atrial weight parameters demonstrated an additional significant effect of dietary sodium intake on tissue weight, independent of animal genetic type. No differences in the relative (GAPDH normalised) expression levels of AT1A- and AT2-receptor mRNA were observed between diet or animal genetic groups.

This study demonstrates that, where there is a pre-existing genetic condition of Ang II-dependent cardiac hypertrophy, the pro-growth effect of elevated dietary sodium intake is selectively augmented. In TG and WT mice, this effect was evident with a relatively short dietary treatment intervention (40 days). Evaluation of the levels of Ang II receptor mRNA further demonstrated that this differential growth response was not associated with an altered relative expression of either AT1A- or AT2-receptor subtypes. The cellular mechanistic bases for this specific Ang II-dietary sodium interaction remain to be elucidated.
Language eng
DOI 10.3317/jraas.2004.036
Field of Research 110106 Medical Biochemistry: Proteins and Peptides (incl Medical Proteomics)
110201 Cardiology (incl Cardiovascular Diseases)
HERDC Research category C1.1 Refereed article in a scholarly journal
Persistent URL http://hdl.handle.net/10536/DRO/DU:30024814

Document type: Journal Article
Collection: School of Exercise and Nutrition Sciences
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