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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Sodium-induced cardiac hypertrophy. Cardiac sympathetic activity versus volume load.

To investigate the possible contributions of cardiac volume overload and cardiac sympathetic hyperactivity in the effects of sodium on cardiac mass, we evaluated the effects of treatment with saline (1%) and deoxycorticosterone acetate + saline (DOCA/saline) for 10 days and 3 and 6 weeks on ventricular anatomy and intracardiac pressures. Sympathetic activity in the heart and other tissues was assessed at 10 days and 3 weeks by catecholamine turnover rates and tyrosine hydroxylase activity. Both saline and DOCA/saline produced concentric left ventricular (LV) hypertrophy. Right ventricular weight showed only small increases. Saline treatment did not affect LV end-systolic pressure, whereas DOCA/saline caused a moderate increase (to 159 mm Hg). Right atrial pressure was not affected by either treatment, whereas LV end-diastolic pressure increased but only after the development of LV hypertrophy. Both saline and DOCA/saline decreased LV norepinephrine concentration; only DOCA/saline decreased norepinephrine content per LV. However, neither treatment altered the norepinephrine turnover rate constant, the absolute turnover rate, or the tyrosine hydroxylase activity. The results demonstrate that increased saline intake or DOCA/saline produces concentric LV hypertrophy without any increase in blood pressure in the case of saline and with increases in LV filling pressure following rather than preceding the appearance of LV hypertrophy. The lack of an increase in LV norepinephrine turnover and tyrosine hydroxylase activity suggests that the hypertrophy is not mediated through increased cardiac neuronal sympathetic activity.[1]


  1. Sodium-induced cardiac hypertrophy. Cardiac sympathetic activity versus volume load. Fields, N.G., Yuan, B.X., Leenen, F.H. Circ. Res. (1991) [Pubmed]
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