Key result
Sodium restriction increases cardiac alpha/beta MHC mRNA ratio independent of the renin-angiotensin system.
Why the study?
The role of the renin-angiotensin system in mediating cardiac myosin heavy chain gene expression adaptations to hemodynamic loads was unclear.
Answers are grounded in this paper and cite their sources.
May inform mechanisms of load-dependent remodeling; leaves open whether renin-angiotensin mediates human cardiac adaptations to pressure overload.
The renin-angiotensin system has been implicated as a possible mediator of the cardiac adaptations that develop in response to chronic pressure overload. In order to explore this, we studied rats that had elevated plasma renin activity (PRA) secondary to 6 weeks of either dietary salt restriction or renovascular hypertension (Htn)--conditions that exert distinctly different loads on the myocardium. Separate groups of sham and Htn animals were maintained on a high salt diet that resulted in a relative (Htn) or absolute (sham) reduction in PRA. Heart weight and heart/body weight ratios were increased only in animals with Htn. The ratio of alpha/beta myosin heavy chain (MHC) mRNA was significantly decreased with Htn. This ratio was markedly increased with low salt and was not influenced by high salt intake. Thus, the circulating renin-angiotensin system does not appear to play a primary role in defining cardiac myosin heavy chain adaptations to hemodynamic loads. However, sodium restriction, either via its hemodynamic or humoral effects, is sufficient to induce a physiologic change in myosin heavy chain gene expression in rats.
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Buttrick et al. (1993) studied Elevated plasma renin activity secondary to dietary salt restriction or renovascular hypertension. Dietary salt restriction or renovascular hypertension vs. Sham and Htn animals on high salt diet was evaluated on Ratio of alpha/beta myosin heavy chain (MHC) mRNA. Sodium restriction significantly increased the ratio of alpha/beta myosin heavy chain mRNA in rat hearts, independent of the circulating renin-angiotensin system.
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