An increase of intracellular potassium and sodium content in the wall of the aorta occurs in experimental renal hypertension. The elevated potassium tends to revert toward normal when blood pressure is again lowered with reserpine. The efficacy of rigid restriction of dietary sodium intake in decreasing blood pressure proved quite limited. The development of renal hypertension in the face of rigid sodium restriction further demonstrates that dietary sodium plays no more than an enhancing role in the pathogenesis of renal “isehemic” hypertension.