Why the study?
Does long-term in vivo sodium depletion increase calcium-activated left ventricular pressure in normotensive rats?
Does long-term in vivo sodium depletion increase calcium-activated left ventricular pressure in normotensive rats?
Long-term in vivo sodium depletion increases maximum calcium-activated left ventricular pressure without altering the sensitivity of the contractile machinery to calcium in a rat model.
Hypothesis-generating in rat models; does not inform clinical sodium management or human cardiac function.
Left ventricular dP/dt has been reported to be enhanced in the perfused isovolumic paced heart (Langendorff preparation) isolated from sodium-depleted rats. In this study, we tested the hypothesis that this positive inotropic effect is caused by increased responsiveness of the contractile myofilaments to calcium. To address this question, the calcium-left ventricular pressure relation during tetanization of the whole heart at different extracellular calcium concentrations (2.5, 5.0, 7.5, 12.5, and 15.0 mM) was studied in 19 sodium-depleted (low sodium diet plus diuretics) and 18 control (regular sodium intake) Sprague-Dawley normotensive rats. Results showed that the maximum calcium-activated left ventricular pressure (induced by tetanization) was significantly higher in sodium-depleted than in control rats at 12.5 mM calcium concentration (170 +/- 27 [SD] mm Hg in sodium-depleted rats vs. 112 +/- 14 mm Hg in control rats, p = 0.0005). The calcium concentration at which half-maximal left ventricular pressure response was attained, however, was not different between the two groups. We conclude that long-term in vivo sodium depletion increased the maximum calcium-activated left ventricular pressure without altering the sensitivity of the contractile machinery to calcium.
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Rossi et al. (1990) studied this question.
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