{'fraction_non_alphanumeric': 0.026727509778357236, 'fraction_numerical': 0.01955671447196871, 'mean_word_length': 5.164658634538153, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Salt sensitive hypertension associated with stem cell defect in the renal medulla of Dahl S rats

Given the importance of the renal medulla in the regulation of sodium excretion and salt sensitivity of arterial pressure, stem cells in the renal medullary niche may contribute to the maintenance of normal cell homeostasis and functional integrity in this kidney region and thereby to the long‐term regulation of arterial pressure. The present study tested the hypothesis that stem cell defect in the renal medulla is involved in salt‐sensitive hypertension in Dahl S (DS) rats due to enhanced local inflammatory response. By immunostaining and flowcytometric analysis, it was found that stem cell marker CD133‐positive cells significantly decreased by 50% in the renal medulla from DS rats vs. control rats. However, pro‐inflammatory cytokine interleukin‐1alpha significantly increased by two folds in response to high salt intake in DS rats vs. control rats. Renal medullary infusion of valproic acid, a stem cell activator, in DS rats for 2 weeks reversed high salt‐induced increase in interluekin‐1alpha and attenuated high salt‐induced increase of arterial pressure (108.1±3.5 mmHg on low salt diet, 148.4±0.2 mmHg on high salt diet and 129±2.8 mmHg on high salt plus valproic acid). It is suggested that stem cell defect may contribute to the renal medullary dysfunction and development of hypertension in DS rats. The protective role of stem cells is associated with their anti‐inflammatory action (support: NIH grant HL‐89563).