Role of sodium in modulation of myocardial hypertrophy in renal hypertensive rats.

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Abstract
To evaluate the role of dietary sodium and antihypertensive drugs in the modulation of myocardial structure, especially myosin isozymic pattern, renal hypertensive rats (two-kidney, one clip) were treated with a sodium-deficient diet (7 mEq/kg), captopril, or atenolol. Native myosin was extracted under nondissociating conditions and separated by polyacrylamide gel electrophoresis. The percentage of myosin isozyme V1 was significantly decreased from 71.5 +/- 7.5 (Wistar controls) to 52.4 +/- 1.7% (p less than 0.05) in renal hypertensive rats and was associated with an increase in V3 component from 12.7 +/- 5.1 (Wistar controls) to 23.1 +/- 1.4% (renal hypertensive rats; p less than 0.05). There was a dramatic change in the myosin isozyme distribution pattern after treatment with low sodium and captopril. Six weeks of low sodium therapy in renal hypertensive rats resulted in an increase in V1 from 52.4 +/- 1.7 to 74.8 +/- 4.8% and a reduction in V3 from 23.1 +/- 1.4 to 9.5 +/- 2.4%. Normal rats treated with low sodium showed similar results. The percentage distribution of isozymes after low sodium therapy in the captopril-treated rats was not different from that in normal Wistar controls. Captopril therapy also caused an increase in V1 and a decrease in V3. Atenolol therapy, on the other hand, caused a significant increase in V3 and decrease in V1 with no change in blood pressure or heart weight. These data suggest that dietary sodium may play an important role in the modulation of myocardial mass and may modulate signals for synthesis of V1 or V3 myosin phenotypes.