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Elevated dietary sodium intake exacerbates myocardial hypertrophy associated with cardiac-specific overproduction of angiotensin II
Enzo R Porrello
Department of Physiology, University of Melbourne, Parkville, Victoria, 3010, Australia
Catherine E Huggins
Department of Physiology, University of Melbourne, Parkville, Victoria, 3010, Australia
Claire L Curl
Department of Physiology, University of Melbourne, Parkville, Victoria, 3010, Australia
Andrea A Domenighetti
Department of Hypertension, University of Lausanne Medical School, Switzerland
Thierry Pedrazzini
Department of Hypertension, University of Lausanne Medical School, Switzerland
Leanne MD Delbridge
Department of Physiology, University of Melbourne, Parkville, Victoria, 3010, Australia, Imd{at}unimelb.edu.au
Trefor O Morgan
Department of Physiology, University of Melbourne, Parkville, Victoria, 3010, Australia
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.
Methods
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.
Results
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.
Conclusion
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.
Key Words: angiotensin II • dietary sodium • cardiac hypertrophy • AT1-receptor • AT2-receptor • transgenic mice
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Journal of Renin-Angiotensin-Aldosterone System, Vol. 5, No. 4,
169-175 (2004)
DOI: 10.3317/jraas.2004.036
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